Shingles Vaccine Protects Seniors and Is Covered by Medicare

Dear Savvy Senior, What can you tell me about the shingles vaccine? I just turned 65 and Have Been Thinking About Getting Vaccinated, but would like to know how effective it is and how it’s covered by Medicare. –Afraid Of Needles Dear Afraid, Older adults get the shingles vaccine WHO can cut whos Their risk of getting the painful condition in half, and Those That do happen to get it are likely to Have a milder case if they’ve Been Inoculated. Here’s what else you should know About the shingles vaccine, how it’s Along With covered by Medicare. Shingles Overview Shingles, herpes zoster Also known as, is a burning, blistering, skin rash Often excruciating That Affects About 1 million Americans each year. The same virus causes chickenpox That causes it. What happens is the chickenpox virus That MOST people get as kids never leaves the body. It hides in the nerve cells near the spinal cord and, for some people, emerge later in the form of shingles. In the U.


S. , one out of every three people will Develop During Their lifetime shingles. While anyone who’s HAD chickenpox can get shingles, it OCCURS MOST Commonly in people over age 60, Along With people Who Have Weakened immune systems. But you can not catch shingles from someone else. Early signs of the disease include pain, itching or tingling before a blistering rash Appears Several days later, and can last up to four weeks. The rash on one side Typically OCCURS of the body, as a band of Often blisters That extends from the middle of your back around to the breastbone. It can Also Appear above an eye or on the side of the face or neck. In Addition to the rash, more than one-third WHO get shingles go on to Develop severe nerve pain can last for months That or even years. vaccination Coverage The Center for Disease Control and Prevention Recommends That everyone age 60 and older Should get a one-time vaccination called Zostavax shingles. Even if you’ve Already HAD shingles, you still need the vaccination Because reoccurring cases are possible. See zostavax. com or call 877-974-4645 for more information or to locate a provider in your area vaccine.

The vaccine is very safe Present. For MOST people the worst side effect is mild redness or soreness arm. Also you need to know That Medicare covers the shingles vaccine as one of Its preventive benefits. But, UNLIKE some other vaccines are paid through That Part B, the shingles vaccination is covered by Part D. If You have a Part D prescription drug plan, it will pay for the vaccine itself and for your physician or other health care provider to give you the shot. You are only responsible for paying the plan’s approved copay at the time you get Vaccinated, Which runs around $ 60 Usually to $ 80. But, you need to make sure you follow your plan’s rules in order to keep your out-of-pocket costs down. If you’re Vaccinated at a drugstore, check to make Certain it’s in your Part D plan network pharmacy. Otherwise, the shot will cost you more than your usual copay. If you’re Inoculated in a doctor’s office, check to make sure the office can bill your plan can work or at Least through a drugstore in your plan’s network. Otherwise, you’ll Have to pay the bill upfront and then a Entire claim reimbursement from your plan. Just to be safe, call your Part D drug plan ahead of time and ask Which pharmacies and doctors in your area you can use to receive the shingles vaccine at the plan’s normal copay. Send your senior questions to: Savvy Senior, P.

O. Box 5443, Norman, OK 73070, or visit SavvySenior. org. Jim Miller is a contributor to the NBC Today show and author of “The Savvy Senior” book. GET THE NEWSLETTER

rash on the primary infection by the human immunodeficiency virus

INTRODUCTION Acute by the human immunodeficiency virus (HIV) infection can cause a courtship of symptoms often go unnoticed despite being a frequent complaint. Among the most prevalent are fever, fatigue and a very characteristic rash that, if recognized, can help establish the diagnosis. This allows early introduction of antiretroviral treatment, which improves the prognosis of the disease and reduces the risk of transmission of this. 4 cases in which the diagnosis of primary infection was suspected from the rash are described. DESCRIPTION OF CASES Case 1 A woman of 49 years with a history of tuberculosis disease in childhood, presented with fever of 38 ° C, sore throat, dysuria, arthralgia, asthenia and a somewhat itchy rash. During scanning erythematous maculopapular, some with central vesiculocostra, not confluent, preferably on the face and upper third of the trunk, with palmoplantar involvement were observed. In the oral mucosa and vulvar ulcers had a fibrin covered, with well defined margins (Fig. 1). In analyzes leukopenia (3,800 cel. / Ul) discreet and elevated liver enzymes glutamic (GOT, 487 U / l) and gamma glutamyl transpeptidase (GPT 258 U / l) was observed.

skin biopsy in which a perivascular lymphohistiocytic infiltrate in the upper dermis, vacuolization of the basal and the presence of some necrotic keratinocytes was performed was observed. He cytology no evidence of herpes infection was demonstrated. Serology of hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein-Barr virus (EBV), HIV, and syphilis were negative. Serology for cytomegalovirus (CMV) and varicella-zoster virus (VZV) demonstrated the existence of an old infection (IgG + and IgM). The general picture and skin lesions resolved spontaneously within a week. An HIV serology practiced 6 months later was positive, so the febrile and other symptoms were attributed to primary infection. The patient, currently performs triple antiretroviral therapy, maintaining levels of CD4> 400 cel. / Ml, with an undetectable viral load and without presenting opportunistic infections. Fig. 1 . — aphthous lesions semimucosa lip and oral mucosa. case 2 A woman of 18, 5 weeks pregnant, went to the emergency room with symptoms of malaise, fever and back pain 5 days of evolution.

and a pathological urinary sediment, a blood test that showed the presence of leukopenia (1500 / ul) and thrombocytopenia (78,000 / ul), along with increased transaminase (GPT 225 U / l GOT, 198 U / l) was performed (> 100 cells / field). Under the tentative diagnosis of urinary sepsis, antibiotic treatment was started. At 24 h of stay in the emergency department began an eruption consists of erythematous maculopapular, not confluent, some with presence of a central vesicle, distributed mainly by the face (fig. 2) and the upper third of the trunk, along with injuries the palms and soles. In the oral and genital mucosa lesions they appeared aphthous appearance. Both symptoms such as mucocutaneous lesions subsided within 10 days. During his hospital stay he had a spontaneous abortion. Serologic testing for HBV, HCV, EBV, HIV, CMV, VZV and syphilis were negative. The cytology of mucocutaneous lesions did not provide relevant data. A skin biopsy in which a perivascular infiltrate was found lymphohistiocytic practiced. Suspecting primary HIV infection determination of plasma HIV RNA was performed, in which 143,000 copies / ml were detected. With the diagnosis of primary infection by HIV, it was established immediately antiretroviral therapy (HAART), being at present with a CD4 count> 500 cel. / Ml and an undetectable viral load.

FIG. 2 . — erythematous papular lesions with vesículocostra. case 3 A 30 year old man addicted to intravenous drugs, with a history of HCV and HBV, and repeated serological tests for HIV-negative consulted by fever have measurable 39 ° C for a week of evolution, to which was added nonpruritic a rash. In the physical examination he revealed erythematous maculopapular rash, distributed by the face and upper third of the trunk. He presented ulcerated lesions in the oral mucosa. a general analysis that were conducted were normal. Determination of proviral DNA confirmed the diagnosis of primary infection by HIV restoring itself of antiretroviral treatment immediately. case 4 A 26 year old woman consulted for a picture of fever, sore throat, joint pain and a non-itchy rash 6 days of evolution. The examination consists of a rash maculopapular orange brown color, not confluent, some with vesiculocostra in the center, distributed mainly on the upper side and the third of the trunk (Fig. 3) was observed.

Also presented aphthous lesions in the gums and soft palate. In analyzes leukopenia (3,840 cel. / Ul) and thrombocytopenia (113,000 cel. / Ul) was observed discrete. In the biopsy of a skin lesion lymphohistiocytic perivascular infiltrate was observed in the superficial dermis. serological tests HBV, HCV, EBV, HIV and syphilis that were negative were performed. CMV serology showed the existence of old infection (IgG + and IgM). Both general symptoms such as skin lesions resolved spontaneously within 10 days. HIV serology at 2 months with negative results repeated. Four years later the patient was admitted to the internal medicine by the appearance of generalized lymphadenopathy one year of evolution. a new HIV serology that was positive was requested. The patient denied risk behavior or mononucleosis syndrome so recent eruption presented 4 years earlier was attributed retrospectively primary infection by HIV. At present, the patient does not follow treatment; it is one of the few patients who do not progress, maintaining a viral load below 400 copies / ml and CD4 approximately> 500 cel.

/ ml, and that have not submitted opportunistic infection. Fig. 3 . — maculopapular lesions, erythematous, violaceous algunasde center. DISCUSSION HIV primary infection may be asymptomatic, but between 50 and 90% of cases have a symptom1. Overall it is a mononucleosis syndrome (fever, lymphadenopathy, etc. ), sometimes so intense that may require hospitalization. This table is known as acute retroviral syndrome and appears as a consequence of the high rate of replication of retroviruses and intense immune response of the individual against the infeccioso2 agent. Symptoms tend to decrease with decreasing load viral1,3. Often they start at 2-4 weeks of infection and are self-limiting in 1 or 2 semanas4. It has been suggested that an intense and prolonged symptoms may be related to rapid progression of disease5. Symptoms that appear most often are fever, fatigue, rash, headache, lymphadenopathy, pharyngitis, joint pain, gastrointestinal symptoms, night sweats and ulcers in the oral and genital mucosa, accompanied in many cases of thrombocytopenia, leukopenia and hipertransaminasemia3 (Table 1) .

Fever and rash are the most common symptoms and probably the most useful for the diagnosis of primary infection by the VIH6,7. The rash usually appears between the first and fifth day of the acute syndrome. This is a non-itchy rash, characteristically distributed by the face and upper third of the trunk, but can spread to the rest of the body surface affecting the palms and soles. Injuries are maculopapular, erythematous-orange, with areas of central necrosis or blistering, oval or rounded, well defined and not confluent. The number between 10 and 100 injuries, and usually measure from a few millimeters to 1 cm diámetro8. Autoinvoluciona rash in about 5-10 days leaving sometimes a thin residual flaking. Patients who developed a superimposable described eruption. It described the emergence of de novo seborrheic dermatitis, 4 or 5 weeks after agudo8 syndrome. In general, it is accepted that there is in 25% of cases concomitant mucosal involvement, although in some series it is found that over 90% of cases the presentan3. Enanthem appear as erosions or, in a more characteristic, ulcers covered grayish-white membrane generally 5-10 mm in diameter, well-defined margins, very painful, reminiscent of a canker sore. They are located on the tongue, palate, gums, lips, esophagus, the genital mucosa and perianal3,7-9 region. Much less frequently they described other skin reactions such as rashes or are pustulosos10,11 vesicular, urticaria difusa12, peeling palms and plantas13, Stevens-Johnson14 and alopecia15 syndrome. The microscopic findings are nonspecific.

Almost always a discrete perivascular lymphocytic infiltrate seen in the superficial dermis, which can be added skin alterations as vacuolization of the basement membrane and the presence of some keratinocyte necrótico16,17. The differential diagnosis is established with organizations that can give a mononucleosis-like syndrome (Table 2). The lack of specificity is one of the reasons why, even today, 90% of cases of primary HIV infection remain diagnosticarse18. The standard technique for the diagnosis of HIV infection is based on detection of antibodies against the virus. Enzimoinmunoabsorción first technique enzyme-linked (ELISA) (very sensitive) and subsequently confirmed by a Western blot (more specific) 19 is performed. Antibody production does not start until 3 to 4 weeks (median 3 months) of infección20, so there is a window period between infection and seroconversion during which detection techniques of antibodies are not tools. To resolve this situation have designed other laboratory tests. The first was the identification of p24, detectable from 14-16 days. Since 1986 it was used in the US as a screening method for blood donors. This is a very specific relatively inexpensive test (99. 96%) and. The problem is its low sensitivity (79%) 21. False negatives appear in patients who initiate the production of antibodies sufficient to neutralize p24 antigen title, yet insufficient to positivize ELISA5 test.

Determining HIV RNA is another technique that becomes positive at 11 days of infection. This is a test designed to monitor response to treatment in patients with known infection. It has a sensitivity of 100% and is accepted as positive when a patient with an acute retroviral syndrome is greater than 50,000 copies / mL viral load. The main drawback is specificity (97%), relatively low if one considers the importance of diagnosis. False positives should be suspected if the viral load is less than 5,000 copies / ml6,22. At present, the most reliable method for the diagnosis of primary HIV infection test is the determination of the proviral DNA in blood leukocytes periférica23. It is performed by a technique of polymerase chain reaction (PCR) and, initially, it was attributed a sensitivity and specificity of 100% 24. Recently, however, they have been described negativos25 false. The diagnosis of primary infection benefit both public health and the individuals affected. People infected after adequate information, should modify their behavior and thus reduce HIV transmission. On the other hand, early introduction of antiretroviral therapy can reduce injuries to the immune system, limit the spread of the virus and reduce the risk of progression disease. 4. Generally it accepted that treatment should be put in place immediately and without interruption through three antirretrovirales26 drugs.

Scientific literature – Open House

Field PR et al, Pathology, 1993, Vol 25, No. 2. Pages 175-179 The Reliability of Serological Tests for the Diagnosis of Genital Herpes: A Critique. Fatahzadeh M \x26amp; Schwartz RA 2007 American Academy of Dermatology Human herpes simplex virus infections: Epidemiology, pathogenesis, symptomatology, diagnosis, and management. Katharine J Looker et al Bulletin of the World Health Organization Vol86 October 2008, 737-816 Estimation of the global prevalence and incidence of infection of herpes simplex virus type 2 Corey L et al The Effects of Herpes Simplex Virus-2 on HIV-1 Acquisition and Transmission: A Review of Two Overlapping Epidemics J Acquir Immune Defic Syndr. 2004; 35 (5) Mahiane SG et al Transmission probabilities of HIV and herpes simplex type 2 virus, effect of male circumcision and interaction: a longitudinal study in a township of South Africa AIDS 2009 – Vol 23 (3) p 377-383 Wald A, Link K. Risk of human immunodeficiency virus infection in herpes simplex type 2 virus-seropositive persons: a meta-analysis. J Infect Dis 2002; 185: 45-52 US Freeman et al. Herpes simplex 2 virus infection Increases HIV acquisition in men and women: systematic review and meta-analysis of longitudinal studies.

AIDS 2006; 20: 73-83 Brown JM, et al. Incident and prevalent herpes simplex type 2 virus infection Increases risk of HIV acquisition Among women in Uganda and Zimbabwe. AIDS 2007; 21: 1515-1523. Wald A, et al. Effect of condoms on Reducing the transmission of herpes simplex virus type 2 from men to women. JAMA 2001; 285: 3100-3106. Corey L, et al. Once-daily valacyclovir to reduce the risk of transmission of genital herpes. N Engl J Med 2004; 350: 11-20 RH ,, Gray et al. Probability of HIV-1 transmission per coital act in monogamous, heterosexual, HIV-1-discordant couples in Rakai, Uganda. Lancet 2001; 357: 1149-1153

Mastro TD, et al. Probability of female-to-male transmission of HIV-1 in Thailand. Lancet 1994; 343: 204-207. Cameron DW et al. Female to male transmission of human immunodeficiency virus type 1: risk factors for seroconversion in men. Lancet 1989; 2: 403-407. Baeten JM et al. Female-to-male infectivity of HIV-1 Among circumcised men and uncircumcised Kenyan. J Infect Dis 2005; 191: 546-553. Boily MC et al. The risk of HIV-1 infection per sexual contact in absence of antiretroviral therapy: a systematic review and meta-analysis of observational studies. 17th International Society for Sexually Transmitted Diseases Research; 29 July-1 August 2007; Seattle, Washington. Weiss et al.


The epidemiology of HSV-2 infection and Its association with HIV infection in four urban African Populations. AIDS 2001; 15: S97-S108. et al. The genital tract immune milieu: an Important determinant of susceptibility and secondary HIV transmission. J Reprod Immunol 2008; 77: 32-40. Corey L. Synergistic copathogens: HIV-1 and HSV-2. N 2007 Engl J Med; 356: 854-856. Schacker T et al Frequency of symptomatic and asymptomatic herpes simplex virus type 2 human immunodeficiency virus reactivations Among men-infected. J Infect Dis 1998; 178: 1616-1622. Nagot N et al. Reduction of HIV-1 RNA levels to suppress therapy With herpes simplex virus. N Engl J Med 2007; 356: 790-799.

Augenbraun M et al. Increased genital shedding of herpes simplex virus type 2 in HIV-seropositive women. Ann Intern Med 1995; 123: 845-847 Siegal FP et al. Severe male homosexuals in acquired immunodeficiency, chronic perianal ulcerative Manifested by herpes simplex lesions. N Engl J Med 1981; 305: 1439-1444. Auvert B et al Randomized, controlled intervention trial of male circumcision for reduction of HIV infection risk: the ANRS 1265 trial. PLoS Med 2005; 2: E298. RH Gray et al. Male circumcision for HIV prevention in men in Rakai, Uganda: a randomized trial. Lancet 2007; 369: 657-666. RC Bailey et al. Male circumcision for HIV prevention in young men in Kisumu, Kenya: a randomized controlled trial.

Lancet 2007; 369: 643-656. Weiss et al. Male circumcision and risk of syphilis, chancroid, and genital herpes: a systematic review and meta-analysis. Sex Transm Infect 2006; 82: 101-109, discussion 110. Auvert B et al Can Prevent male circumcision acquisition of HSV-2 infection? In: 16th Biennial Meeting of the International Society for Sexually Transmitted Diseases Research; 10 to 13 July 2005; Amsterdam, The Netherlands; 2005. A Tobian et al. Trial of male circumcision: prevention of HSV-2 in men and vaginal infections in female partners, Rakai, Uganda. In: 15th Conference on Retroviruses and Opportunistic Infections; 3-6 February 2008; Boston, Massachusetts; 2008. National HIV and Syphilis Report Prevalence Survey South Africa 2006 Pretoria, South Africa: Department of Health; 2006. pp. 1-31. Auvert B et al Can highly active antiretroviral therapy reduces the spread of HIV?

A study in a township of South Africa. J Acquir Immune Defic Syndr 2004; 36: 613-621. J Carpenter, J. Bithell Bootstrap confidence intervals: when, Which, what? A practical guide for medical statisticians. Stat Med 2000; 19: 1141-1164. R Development Core Team. R: a language and environment for statistical computing. Vienna, Austria: R Foundation for Statistical Computing; 2005. Mastro TD, Kitayaporn D. HIV type 1 transmission probabilities: estimates from epidemiological studies. AIDS Res Hum Retroviruses 1998; 14: S223-S227. Auvert B et al.

Among youth HIV infection in a South African mining town is Associated With Herpes Simplex Virus-2 seropositivity and sexual Behaviour. AIDS 2001; 15: 885-898. Auvert B et al. Ecological and Individual level analysis of risk factors for HIV infection in four urban Populations in sub-Saharan Africa With different levels of HIV infection. AIDS 2001; 15: S15-S30. Buve A, et al. The multicentre study on factors Determining the differential spread of HIV in four African cities: summary and conclusions. AIDS 2001; 15: S127-S131. Celum C Connie et al. HSV-2 suppressive therapy for prevention of HIV acquisition: results of HPTN 039 [abstract 31499]. In: 15th Conference on Retroviruses The Opportunistic Infections and; 3-6 February 2008; Boston; 2008.

Cold Sores Treatment PDF

How to Cure Genital Herpes Virus Treatment Male And Female Genital Herpes – Part 4 Navigation Return to Content Cold sores are caused by a few simple virus infectious diseases, depending on the location of herpes be more or less severe. What is the same for all, it is the enormous discomfort that produces suffering that condition. Here I have a treatment for PDF . . . Cold Sores Cold sores are a very annoying ailment, the [. . . ] Keep reading.

. . When we hear the word herpes a chill ran down our backs, traditionally with only mentioning this concept the reaction of people is of rejection, fear, and why not say, disgust. This negative response to herpes is very counterproductive for those affected, who live episodes of confusion, loneliness and social inscrutability, embarrassed by [. . . ] Keep reading. . . There are many home remedies for genital herpes that can be drawn, then this article will name the most useful. >> Home remedies for inflammation and itching of the genital herpes by applying cold. That is to apply cold in the affected area, but should not be applied [.

. . ] Keep reading. . . When cure herpes zoster effectively, we can use a lot of advice, for example, we recommend the use of green tea, which, if used in conjunction with powdered moringa leaves, will give great results in preventing, soften and combat those effects and discomfort that can generate the [. . . ] Keep reading. . .


Treatment for female genital herpes should be applied from the moment the patient begins to suffer the first symptoms, so as soon as possible to tackle the disease and the effects are minor. Among the types of treatments there are several solutions. For example, one of those who often recommend [. . . ] Keep reading. . . Genital herpes is a sexually transmitted disease that results from infection with a virus called herpes simplex virus type 2 (HSV2). There are several ways for you to lead a normal life and relieve symptoms when outbreaks occur. What to expect from treatment of genital herpes Although there are people who [. .

. ] Keep reading. . . Genital herpes is caused by herpes simplex virus. Pustules, also known as sores, are caused by this virus. The herpes simplex virus has two modes called, herpes simplex virus 1 and herpes simplex virus 2. Most people believe that herpes simplex 1 [. . . ] Keep reading.

. . Hello and thanks for visiting our blog ComoCurarHerpesGenital. com, Victor and Magaly We are ex-patients Genital herpes, Lip and Zoster and we decided to create this blog to advise, guide and make known that if there is an effective treatment for Herpes Cure your body. Today we will share with you our story of how we free [. . . ] Keep reading. . . Once I had the opportunity to study physician hablal with a post-graduate at the Faculty of naturopathic medicine 4 years. The taught me that there are treatments than any other conventional medical ever learn.

Therefore, he says that the body has the ability to heal itself. Also told me that [. . . ] Keep reading. . . Vaginal candidiasis and herpes have similar symptoms. Vaginal infection is very common among women. In fact, 3 of 4 women will suffer from an episode of vaginal infection or more in their lives. Vaginal herpes or genital herpes is less common but spreads rapidly. About 25% of the [.

. . ] Keep reading. . . ComoCurarHerpesGenital. com

International journal of odontostomatology – Virus in Endodontics

Virus in Endodontics Viruses in Endodontics Scarlette Hernández Vigueras *; Luis Salazar Navarrete **; Ricardo Perez Tomas ***; Juan José Segura Egea ****; Miguel Viñas ***** \x26amp; José López-López ****** * Faculty of Medicine, Universidad Austral de Chile, Valdivia, Chile. PhD Dental Sciences, Campus Universitario de Bellvitge, University of Barcelona, ​​Spain.  ** Laboratory of Molecular Biology and Pharmacogenetics, Department of Basic Sciences, Faculty of Medicine, University of La Frontera, Temuco, Chile.  *** Full Professor. Department of Basic Sciences. Campus Universitario de Bellvitge. University of Barcelona, ​​Spain.  **** Full Professor. Department of Stomatology. University of Sevilla, Sevilla, Spain.

 ***** Laboratory of Molecular Microbiology and Antimicrobials. Department of Pathology and Experimental Therapeutics, University of Barcelona, ​​Spain.  ****** Professor of Oral Medicine. Odontoestomatología Department, Campus Universitario de Bellvitge, University of Barcelona, ​​Spain. Mailing Address: SUMMARY: The endodontic infection is the infection of the root canal system and undoubtedly is the main etiological agent of apical periodontitis. Further, endodontic pathogenic bacteria, has been sought in recent years to associate the presence of viruses in different types of endodontic pathology. Viruses that have been searched and associated are those belonging to the herpesvirus family, which are found mainly present in periapical pathologies. It has also sought to relate its presence pathologies with more symptoms, or radiographic image presented periapical bone destruction older. The role of viruses in the apical lesions of endodontic origin is still unclear, we speak of cumulative those of bacteria, in addition to possible local immunosuppression that would favor growth and the effect of the latter effects. KEYWORDS: herpesvirus, human papilloma virus, cytomegalovirus, Epstein-Barr, apical periodontitis, endodontic infection, endodontics virus. ABSTRACT: Endodontic infection is an infection of the root canal system and is the main etiological undoubtedly agent of apical periodontitis. In recent years, research has Aimed to associate the presence of virus and endodontic bacterial pathogens in the different types of endodontic disease.

The most common viruses That Have Been Associated researched and are members of the herpesvirus family, Which are mainly present in periapical pathologies. Furthermore, research has-been Carried out Relating to Their presence pathologies With Important symptoms, or radiographic imaging Those shows EXTENSIVE Where apical bone reabsorption. The role of viruses in apical lesions of endodontic origin are still unclear, it hypothesizes the cumulative effect With bacteria, in Addition to Local possible immunosuppression That favors the growth and the effect of bacteria. KEY WORDS: Herpes virus, human papillomavirus, human cytomegalovirus, Epstein-barr virus, apical periodontitis, endodontic infection, endodontic. INTRODUCTION Endodontic infection is defined as infection of the root canal system and undoubtedly is the main etiological agent of apical periodontitis. chemical and physical factors can induce periapical inflammation, but the microbiological factor is essential for this inflammation can persist and progress (Siqueira \x26amp; Rocks, 2009). Apical periodontitis or periapical lesions, the inflammatory disease is affecting the surrounding tissues of the apical portion of the tooth, causing destruction of these tissues (Graunaite et al, 2012;. Siqueira \x26amp; Rocks). These polymicrobial infections may have an acute or chronic course, and have various manifestations or clinical and radiographic features. The type of response or clinical characteristics variation may be due to different microbiological profiles that arise, or to the host immune response (Slots et al. , 2004). Currently, the consensus classification of the American Association of Endodontists (Glickman, 2009) is used, that in speaking of apical periodontitis, distinguished: i) Symptomatic, they can go or not accompanied by a periapical radiolucent area.

ii) Asymptomatic which, appearing as a periapical radiolucent area, but not accompanied by any clinical symptoms. The impact of apical periodontitis is not only at the level of oral cavity, but also in its possible relationship to various diseases or systemic conditions such as type 2 diabetes (López-López et al. , 2011) or snuff and hypertension (Segura-Egea et al. , 2011), among others. Over 500 species of microorganisms colonize the oral cavity, but only 15 to 30 are those which are frequently detected in infected channels may be responsible for most apical periodontitis in immunological-logically competent individuals. Another fewer species may be involved in other cases, particularly in cases of endodontic failures post (Siqueira \x26amp; Rocks). Viruses are cancerogénicos ulcerogenic agents and in the oral cavity and infestation is common in the mucosa and perioral area. Oral pathologies that are related to viral agents are oral ulcers, tumors and other diseases such as lichen planus and marginal periodontitis among others. Therefore, in recent years it has been sought to relate various viruses, and the specific bacteria, with symptomatic and asymptomatic apical periodontitis, using for techniques detection immunohistochemistry and detection in polymerase chain (PCR) (Li et al. , 2009; Sabeti et al. , 2003; Saboia-Dantas et al, 2007). . In recent years, attention has focused studies on the detection of virus of the herpesvirus family.

In particular, the studies focus on Epstein Barr or VHS-4 (EBV), Cytomegalovirus or VHS-5 (CV) and Herpes simplex (HSV 1 and 2) virus. However, Ferreira et al. (2011) sought and detected in samples of purulent exudate of acute apical abscesses, the presence of other viruses belonging to the herpesvirus family, like the VHS-6 and VHS-8, in addition to search and detect the presence of human papilloma virus. Endodontic pathologies associated virus. Herpesviruses or viruses belonging to the Herpesviridae family, are one of the major viral families present in the oral cavity. They are DNA (double straight chain) virus and herpesvirus virion size varies 120-150 nm. They have an icosahedral capsid, proteinaceous tegument and an envelope with viral glycoproteins. 8 types of species of human herpesviruses are known: herpes simplex 1 (HSV-1), herpes simplex 2 (HSV-2), Varicella-zoster virus (VZV) or herpes virus 3, Epstein-Barr virus (EBV) or herpesvirus 4 cytomegalovirus (CMV) or herpes virus 5, herpesvirus 6 (HHV-6), 7 (HHV-7) and 8 (HHV-8). Each of these viruses differ in biological and clinical characteristics (Slots, 2009). HSV-1 and 2 has been sought in several studies, however, none is presented with a statistically significant difference, isolated cases occur, suggesting that these viruses would not be associated with a potential role in endodontic diseases ( Chen et al, 2009;. Ferreira et al . ; Heling et al. , 2001; Li et al .

; Rosaline et al, 2009;. Sabeti et al, 2003a;. Sabeti et al, 2003b;. Sabeti \x26amp; Slots, 2004 ; Sabeti et al 2003c). . In turn, the VZV has been sought in three studies, which appear present in a very low number of samples, even a case that appeared this, it was finally associated with a misdiagnosis of herpes zoster, which presented similar symptoms to symptomatic irreversible pulpitis (Chen et al . ; Ferreira et al . ; Li et al. ). HHV-4 or EBV is one of the most commonly been associated in studies endodontic pathology, being present in a significant number of samples compared to healthy control groups (Chen et al . ; et al . ; Hernádi Ferreira et al. , 2010; Li et al .

; Ozbek et al, 2013;. Rosaline et al . ; Sabeti et al, 2012;. Sabeti et al, 2003a, 2003b, 2003c;. Sabeti \x26amp; Slots, 2004; Saboia-Dantas et al. ; Slots et al . ; Sunde et al, 2008;. Yazdi et al, 2008;. Yildirim et al, 2006). . HHV-5 or Cytomegalovirus (CMV) also along EBV is one of the most studied (Andric et al. , 2007; Chen et al . ; Ferreira et al .

; Hernádi et al, 2010;. Li et al . ; Rosaline Ozbek et al . ; et al. ,; Sabeti et al, 2012;. Sabeti et al, 2003a, 2003b, 2003c;. Sabeti \x26amp; Slots, 2004; Saboia-Dantas et al Slots et al . ; Sunde et al. . ; Yazdi et al . ; Yildirim et al. ); however, in studies in which it appears present in samples endodontic pathology no statistically significant compared with control group difference (Hernádi et al, 2010;. .

Li et al), so its potential role in endodontic pathology is controversial. The main viral association was found in studies of CMV and EBV is present in almost one third of the samples with endodontic pathology studied (Hernádi et al, 2010;. . Li et al . ; et al . ; Sabeti Ozbek et al, 2012; Sabeti et al, 2003a, 2003b, 2003c;. Sabeti \x26amp; Slots. , 2004; Saboia-Dantas et al Slots et al . ; Sunde et al . ; Yazdi et al . ; Yildirim et al. ). In primary teeth with periapical pathology has also been evaluated for the presence of these viruses in a total of 12 samples, the EBV is present in 8 and CMV in 7 statistically significant when compared with the control group (healthy premolars extracted for reasons difference orthodontic) (Yildirim et al.

). With respect to the detection of HHV-6, two studies have looked for this virus. Hernádi et al. (2011), which was detected in 8 of 40 samples of periapical lesions, and Ferreira et al. their presence detected in 2 of 33 samples of acute apical abscesses. Ferreira et al. , Also studied the presence of HHV-7 and HHV-8 in acute apical abscesses, finding HHV-7 in only a sample of apical abscesses and in a control instead albuscar HHV-8, found that in 18 of the 33 samples abscesses, it appeared virus present. The presence of this virus population is strongly associated with HIV (+), however, patients in the study, none was HIV (Ferreira et al. ). HPV belongs to the Papillomaviridae family, it is a double-stranded virus DNA, circular, which have identified more than 120 types. It is a small virus, has epithelial tropism and no envelope. In humans they have been associated with a variety of proliferative epithelial lesions, even been associated with premalignant or malignant conditions (Kumaraswamy \x26amp; Vidhya, 2011). However we found few studies that detect its presence associated with endodontic pathology, most recently, associates it with acute apical abscesses (Ferreira et al.

), Resulting positive in 3 of the 33 samples of purulent exudate. Virus and its relationship with the symptoms and the size of the root apical lesions. You searched correlate the presence of specific viral agents with endodontic disease that causes symptoms such as swelling, pain, tenderness to biting, tenderness or percussion. Viruses that have appeared associated with this type of injury are the Epstein-Barr virus and Cytomegalovirus, alone or in combination (Sabeti et al, 2003c, 2012;. Sabeti \x26amp; Slots, Slots et al. ). However, other studies have not found any statistically significant difference when comparing the viral presence among apical periodontitis symptomatic and asymptomatic ratio (Andric et al . ; Hernádi et al, 2010;. Li et al . ; Ozbek et al. ). Regarding the presence of virus by size of the apical lesion, the results differ. Sabeti et al.

(2003a), Sabeti \x26amp; Slots and Hernádi et al. (2010, 2011) will encuentraron a relationship between the presence of EBV, CMV and HHV-6 subtype B virus in large apical lesions. Conversely Li et al. found no statistically significant difference. Currently, lack describe the role of viruses in periapical lesions, postulating possible additive effects of the presence of virus, more endopatógenas bacteria and activation of proinflammatory immune mechanisms that may manifest in an increase periapical resorption and clinical symptoms . The virus can cause local immunosuppression, which favors bacterial growth in the periapex. On the other hand the virus may be present and replicate in humans, but without causing symptoms, so care must be taken when considering the clinical relevance of viral presence. It is important to know and understand the new microbiological interactions that occur in endodontic diseases, which could shed light for new therapeutic approaches, seeking to improve the prognosis of therapies. BIBLIOGRAPHIC REFERENCES Andric, M . ; Milasin, J . ; Jovanovic, T. \x26amp; Todorovic, L.

Human cytomegalovirus is present in odontogenic cysts. Oral Microbiol. Immunol, 22 (5):. 347-51, 2007. [Links] Chen, V . ; Chen, Y . ; Li, H . ; Kent, K . ; Baumgartner, J. C. \x26amp; Machida, C. A.

herpesviruses in abscesses and cellulitis of endodontic origin. Endod J. , 35 (2):. 182-8, 2009. [Links] Ferreira, D. C . ; Rocks, I. N . ; Paiva, S. S . ; Carmo, F. L .

; Cavalcante, F. S . ; Rosado, A. S . ; Santos, R. \x26amp; K. Siqueira, J. F. Jr. in Viral-bacterial acute apical abscesses associations. Oral Surg. Oral Med. Oral Pathol.

Oral Radiol. Endod, 112 (2):. 264-71, 2011. [Links] Glickman, G. N. AAE Consensus Conference on Diagnostic Terminology: background and perspectives. Endod J. , 35 (12):. 1619-1620, 2009. [Links] Graunaite, I . ; Lodiene, G.

\x26amp; Maciulskiene, V. Pathogenesis of apical periodontitis: a literature review. J. Oral Maxillofac. Res, 2 (4). E1, 2012. [Links] Heling, I . ; Morag-Hezroni, M . ; Marva, E . ; Hochman, N . ; Zakay-Rones, Z. \x26amp; Morag, herpes simplex virus A.


Is Associated With pulp / periapical inflammation? Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod, 91 (3):. 359-61, 2001. [Links] Hernádi, K . ; Csoma, E . ; Adam, B . ; Szalmás, A . ; Gyöngyösi, E .

; Veress, G . ; Ildikó-Márton, I. \x26amp; Kónya, J. Association of human herpesvirus 6 symptomatic apical periodontitis With subtypes. Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod, 112 (3):. 401-6, 2011. [Links] Hernádi, K . ; Szalmás, A .

; Mogyorósi, R . ; Czompa, L . ; Veress, G . ; Csoma, E . ; Marton, I. \x26amp; Kónya, J. PrPrevalence and activity of Epstein-Barr virus and human cytomegalovirus in symptomatic and asymptomatic apical periodontitis lesions. Endod J. , 36 (9):. 1485-9, 2010. [Links] Kumaraswamy, K. L.

\x26amp; Vidhya, M. Human papillomavirus and oral infections: an update. J. Cancer Res Ther, 7 (2):. . 120-7, 2011. [Links] Li, H . ; Chen, V . ; Chen, Y . ; Baumgartner, J. C. \x26amp; Machida, C.

A. herpesviruses in endodontic pathoses: association of Epstein-Barr virus With irreversible pulpitis and apical periodontitis. J. Endod, 35 (1):. 23-9, 2009. [Links] Lopez-Lopez, J . ; Jané-Salas, E . ; Estrugo-Devesa, A . ; Velasco-Ortega, E . ; Martin-Gonzalez, J. \x26amp; Segura-Egea, J. J.

periapical and endodontic status of type 2 diabetic Patients in Catalonia, Spain: a cross-sectional study. Endod J. , 37 (5):. 598-601, 2011. [Links] Ozbek, S. M . ; Ozbek, A. \x26amp; Yavuz, M. S. Detection of human cytomegalovirus and Epstein-Barr Virus in symptomatic and asymptomatic apical periodontitis lesions by Real-time PCR. Med. Oral Pathol.

Oral Cir. Buccal, 18 (5): e811-6, 2013. [Links] Rosaline, H . ; Satish, S. \x26amp; E. Kandaswamy, D. Detection of presence or absence of herpes simplex virus, Epstein Barr virus and human cytomegalovirus in infected pulp using a polymerase chain reaction. Aust. Endod. J. , 35 (1): 9-12, 2009. [Links]

Sabeti, M . ; Kermani, V . ; Sabeti, S. \x26amp; Simon, J. H. Significance of human cytomegalovirus and Epstein-Barr virus in inducing cytokine expression in periapical lesions. J. Endod, 38 (1):. 47-50, 2012. [Links] Sabeti, M . ; Simon, J. H .

; Nowzari, H. \x26amp; Slots, J. Cytomegalovirus and Epstein-Barr virus active infection in periapical lesions of teeth With intact crowns. Endod J. , 29 (5):. 321-3, 2003a. [Links] Sabeti, M . ; Simon, J. H. \x26amp; Slots, J. Cytomegalovirus and Epstein-Barr virus are symptomatic periapical Associated With pathosis. Oral Microbiol.

Immunol, 18 (5):. 327-8, 2003b. [Links] Sabeti, M. \x26amp; Slots, J. herpesviral-bacterial coinfection in periapical pathosis. Endod J. , 30 (2):. 69-72, 2004. [Links] Sabeti, M . ; Valles, Y . ; Nowzari, H .

; Simon, J. H . ; Kermani-Arab, V. \x26amp; Slots, J. Cytomegalovirus and Epstein-Barr virus DNA transcription in symptomatic endodontic lesions. Oral Microbiol. Immunol, 18 (2):. 104-8, 2003c. [Links] Saboia-Dantas, C. J . ; Coutrin Toledo, L. F .

; Sampaio Filho, H. R. \x26amp; Siqueira, J. F. Jr. herpesviruses in asymptomatic apical periodontitis lesions: an immunohistochemical approach. Oral Microbiol. Immunol, 22 (5):. 320-5, 2007. [Links] Segura-Egea, J. J . ; Castellanos-Cosano, L .

; Velasco-Ortega, E . ; Rios-Santos, J. V . ; Llamas-Carreras, J. M . ; Machuca, G. \x26amp; López-Frías, J. F. Relationship Between smoking and endodontic variables in hypertensive Patients. Endod J. , 37 (6):. 764-7, 2011. [Links]

Siqueira, J. F. Jr. \x26amp; Rocks, I. N. Distinctive features of the microbiota Associated With Different forms of apical periodontitis. J. Oral Microbiol. , 1: 10. 3402 / jom. v1i0. 2009, 2009. [Links]

Slots, J. Oral viral infections of adults. Periodontol. 2000, 49: 60-86, 2009. [Links] Slots, J . ; Nowzari, H. \x26amp; Sabeti, M. Cytomegalovirus infection in symptomatic periapical pathosis. Int. Endod. J. , 37 (8): 519-24, 2004.

[Links] Sunde, P. T . ; Olsen, I . ; Enersen, M . ; Beiske, K. \x26amp; Grinde, B. Human cytomegalovirus and Epstein-Barr virus in apical and marginal periodontitis: a role in pathology? J. Med Virol, 80 (6):. . 1007-1011, 2008. [Links]

Yazdi, K. A . ; Sabeti, M . ; Jabalameli, F . ; Eman Eini, M . ; Kolahdouzan, S. A. \x26amp; Slots, J. Relationship Between human cytomegalovirus transcription and symptomatic apical periodontitis in Iran. Oral Microbiol. Immunol, 23 (6):. 510-4, 2008. [Links]

Yildirim, S . ; Yapar, M . ; Kubar, A. \x26amp; Slots, J. Human cytomegalovirus, Epstein-Barr virus and bone resorption-inducing cytokines in periapical lesions of deciduous teeth. Oral Microbiol. Immunol, 21 (2):. 107-11, 2006. [Links] Funds of the Research and Development, Universidad Austral de Chile, Chile, Project DID S-2012-05. Mailing Address: Scarlette Hernández Vigueras Institute Odontoestomatología

 Austral University of Chile  Rudloff 1640, Valdivia  CHILE Email: shernandez@uach. cl Received: 27/03/2014  Accepted: 23/07/2014

Antidote against the parasite Chikungunya

I. WHAT IS CHIKUNGUNYA? The name comes from the Macondo Chikungunya language in Tanzania; this name refers to “one who stoops” referring to the position that causes the microbe to infect people, which is associated with arthritis-like symptoms. The infectious agent Chikungunya is a micro-parasite hatched from eggs hatched in an insect, which previously fed with human blood contaminated with Plasmodium parasites previously undergone genetic reengineering to penetrate faster the cells and when they leave their eggs from the insect exceed the defensive capacity of the human immune system. When speaking of Chikungunya Virus actually eggs micro-parasite alluded. A eggs of the micro-parasite has labeled them with the name of Chikungunya Virus -CHIKV-. A representation of the micro-parasite shown in Diagram No. 1. Diagram No. 1. (Photo of micro-parasite Chikungunya. Source Dr. R.

K. Gupta) Eggs micro-parasite belong to the typology of Alphavirus, they are the result of genetic engineering of viral recombination used to produce this construct laboratory and these infectious agents are classified into the chimeric viruses, as part of its DNA has been replaced with human DNA sequences, having incorporated an epidermal growth factor receptor (EGFR, for its acronym in English) to be spread quickly through the skin to the entire body. A representation of the construct of CHIKV shown in the diagram No. 2. Diagram No. 2. (Representation of the structure of the egg or the Chikungunya virus. Source: R. J. Microbiol Rev. 1994 Kuhn) Virus Chikungunya micro-parasite is made with specific genes or amino acid substitutions in chromosomal segments plasmodium parasites.

The change in the amino acids can act through multiple phenotypic effects to create an epidemic situation where innocent human populations are involved, both arthropod-borne viruses such as infectious diseases evolving in humans. PROVENANCE OF AGENT II CHIKUNGUNYA In 1952 scientist Thomas Weller, working for the US military developed the technique to extract large amounts of eggs Chickenpox and Shingles from the roundworm parasites. The same technique was used to produce new parasites eggs plasmodia variants previously fed Herpes simplex radioactively loaded and placed playing in a mixture of blood and calf kidneys amniotic fluid of pregnant women. When plasmodia excrete their eggs in the mix, then were put to insects, mosquitoes and ticks, they suck out. These new eggs plasmodia opened inside the insect and gave rise to a class of more aggressive parasite by its infectiousness. Insect eggs born, understand the new variant have been called chikungunya virus, which were scattered in towns of Tanzania in 1952, the first report appears in 1955, written by Marion Robinson and W. H. R. Lumsden ( “An Epidemic of Virus Disease in Southern Province, Tanganyika Territory, in 1952-53” Part I and II Transactions of the Royal Society of Tropical Medicine and Hygiene 1955; 49:. . . 28-32 and 49: 33-57 ).

The refinement of engineering viral recombination using parasites interact to produce eggs chikungunya, has enabled today the mosquito, ticks or other insects and invertebrates have been replaced, as a vector of transmission, vertebrates such as chicken, mice, monkeys and all kinds of mammals or birds. The main means of spread of eggs or virus chikungunya obtained by recombination of Plasmodium parasites are aerosols or different means of spraying and fumigation, also foods that come from animals, water and containers that have been contaminated planned manner with the pathogen chikungunya. III. -MAP GENOME STRUCTURE CHIKUNGUNYA A genetic analysis of egg cartogram chikungunya – CHIKV- shows that genetic engineering of CHIKV was to insert chromosomal segments or nucleotide sequences in DNA plasmodium genes based on eight different types of parasites and bacteria and incorporating plasmodia those segments of human genes related regulator of epidermal growth factor (EGFR). The genes of viruses, parasites and bacteria inserted into the genome of Chikungunya are predominantly the following: the Human Papillomavirus (HPV), the bacteria Ureaplasma urealyticum (Urea. U), the polio virus cytomegalovirus (CMV), macro PARASITE Fasciola hepatica (F. hepat. ), spores Drosophila (Drosoph. ), human immunodeficiency Virus (HIV), Escherichia coli (E. coli) bacteria Psudomona putida (Ps. Put. ) and dengue .


The construct of CHIKV has four segments Nonstructural Proteins (NSP) and five structural segments, with insets of genes of pathogens such as seen in diagram # 3. Diagram No. 3 (Reconstruction of the structure of CHIKV Cf: October 25 Virology 2009; 393 (2):. . 183-197). The pathogen Chikungunya is inserted at the end or 5’domain, I related to nsp1 segment gene sequences Human Papillomavirus (HPV), so that the virus, serving as activator of initiation of synthesis of -RNA and grabber genome RNA transcription of the cell infected by the microparasite or plasmodium, in the process of transferring the abnormal code to the human cell, develop or activate latent herpes infections, fungi, Candida albicans and others in the mouth, vaginal cavity and testicles. In the nsP2 segment of the pathogen CHIKV is inserted genetic information of the bacteria Ureaplasma urealyticum (UU), which inhibits cell proteins, ensures maximum expression of the viral genome and manages to evade the immune response of the host invaded in this case the human being, causing impaired fertility, as well as cardiovascular and lymphatic system in the person. The nsP3 segment contains particles or nucleotides from the Virus cytomegalovirus (CMV), which alter the transfer of magnesium and phosphate to the host cell, causing an aberrant or abnormal phosphorylation in infected cells and causing the viral RNA is negative, allowing altered RNA synthesized is low infection in cells at 40 ° C. CMV actually triggers pseudomitosis processes during infection to humans, which is similar to cell mitosis but involves the formation of multiple fuzzy poles, abnormal condensation and translocation of chromosomes of DNA. The consequences of the interaction of genetic information contained in this nsP3 segment of CHIKV are seen in disorders in the lympho-reticular tissue, dendritic cells receiving joints, secretory glands, kidneys and other tissues; cancer patients and ailments are at greater risk of syndromes caused by CMV genes inserted in the CHIKV, including pneumonia, gastrointestinal infections, mental retardation, hearing loss, hepatitis, retinitis and encephalitis. The nsP4 segment has been formed primarily from infectious proteins extracted from macroparásito Fasciola hepatica, whose larvae are fed previously contaminated with radioactive amino acids. The main amino acid of this kind of products of excretion and secretion -ESP, for its acronym in English is common to all alphavirus, radioactive thyroxine (tyrosine) which together form carcinogenic phosphates pictures. These genes nsP4 are designed so that the mutant can not suspend the synthesis of fewer chains not permitted temperatures, understand, still replicate even in boxes fever infected.

These proteins tend to degrade the signal by a long amino acid complex, among which there stabilizers or promoters activity viral synthesis of this agent (methionine and alanine) and other amino acids that affect or destabilize (phenylalanine, leucine, arginine , lysine, aspartic acid and glutamic acid). The segment Capsid Protein (capsid protein) is derived from genes spores Drosophila and fits in the nascent protein structure, forming an icosahedral core structural particles, resulting in the encapsulated core, to permit maturation of virions, the which adhere to the infected cell membrane and fuses with that of the cell, from which release encapsulated core and into the cytoplasm occurs. Based on the information of the Drosophila larvae emerge carnivorous logically voraciously to human tissues. The content of the genes of the E3 segment has remained well reserved for that is not known by the scientific world and less for human beings affected by the pandemic Chikungunya, as corresponding to genes extracted from a parasite whose origin unnatural is it has been shown in multiple scientific papers and in judicial proceedings against those who prepared. E3 segment of the Chikungunya has inserted HIV genes, why it would explain that the immuno-compromised population including patients with transplants, transfusions, HIV / AIDS and especially patients suffer from cancer and reactivation or recurrence them these diseases, is the most affected and even death. CHIKV E2 segment is responsible for the viral agent fits into host cells and consists of structural proteins from Escherichia coli bacteria, responsible for symptoms of severe nausea, vomiting and severe stomach pains. The 6K segment of bacterial CHIKV virus contains genes from the bacterium Pseudomonas putida, the same that has been used in sausages and canned to avoid the stench of putrefaction of these products when they follow the decomposition process having already been packaged. This segment is a constituent 6K protein related viral membrane glycoproteins processing, cell permeabilization and asexual reproduction of viral particles. This ensures 6K segment elevation cytoplasmic calcium and influences the selection of lipid domains that interact with glycoproteins layers. Chikungunya contains the pathogen at the end or 3’domain, related to the E1 segment gene sequences from dengue. This segment consists of a class of viral fusion protein. E1 segment promotes the distribution of nucleocapsids into the cytoplasm, then endosomes and fusion of the viral membrane. The more cholesterol is present in the membrane, greater efficiency is achieved in viral fusion.

the reason why diabetic patients suffer more intensely attack the infectious agent Chikungunya and symptoms of the infection thus comprises are similar to those shown when dengue has contaminated an individual. The methods and techniques more advanced genetic reengineering today for a viral construct as refined with the pathogen Chikungunya, far from being a literary fiction, are recorded in international organizations that handle patents. In such patents is presented to the Chikungunya virus as progress in its infectiousness compared to Semliki Forest virus, the virus equine encephalitis in Venezuela, the CHIKV La Reunion and other heterologous alphavirus. A patent for the manufacture of infectious clones of Chikungunya was awarded to the University of Texas, but rights reserved to the US Government in 2010 under No. US 20100233209A1. Another patent to manufacture chiméricos Chikungunya virus and its subsequent use was granted in July 2011, under No. US 20110171249. An extension of the earlier patent was authorized in January 2013 under No. US 8343506B2. It is considered necessary to relieve that such patents referred to laboratory confirmed on infectious diseases, from which documents it is clear that although there is a great affinity of CHIKV into cells receptor as mammals and mosquitoes, consider strongly the suggestion, according to which the infectious virus Chikungunya route is via aerosols. It is also referred to in these patents was already known in 1981 the conversion of this virus into a lethal weapon by the armed US forces and to the governments of Germany and Austria, this virus Chikungunya, is considered as a biological weapon . IV. -THE CURE AGAINST THE PARASITE CHIKUNGUNYA

Conventional medicine makes treatment protocols based on indications of foreign laboratories and unknown remote regions of infectious foci and the most affected populations. An effective conventional treatment protocol to eliminate the infectious agent Chikungunya human body still has not been presented, but only mitigating measures. Nanoscience offers cutting-edge solutions, which are the only antidote against the parasite Chikungunya, based on four CHIKV weaknesses: the segments (i) nsP2 with Urea. U. , (ii) nsP3 with CMV, (iii) nsP4 with F . hepat. , and (iv) 6K with Ps. putida. Parallel to the implementation of nanotherapies, general prophylactic measures are also prescribed, which are oriented towards removing items from animals, mainly chicken and processed foods from non-plant origin. 1. -treatments with nanoparticles accessible extracts from plants: If nanoparticles plants are extracted with high energy solvent heavy metal or droppings parasites and these nanoparticles are ingested in high tolerable temperatures for the human organism, thermal fields that degrade the electrical signal of genes of bacteria are created, inserted in nsp2 and 6K, Ureaplasma urealyticum and Pseudomonas putida. To achieve battle against the genes of both just take five glasses a day for twelve weeks malojillo potions with lemon juice and honey.

If you want to remove the infectious genes inserted into the nsP3 from CMV, would be enough to take seven glasses a day for four weeks potions boiled with tamarind nugget, tangerine peel and green leafy vegetables or legumes. If you want to cancel the activity of genes nsP4 hepatic segment derived from Fasciola, you only have to alternate two concoctions: six cups daily for twelve weeks of the boiling concoction machine, sweet wormwood and cloves; then five daily cups of another potion liquefying heart of tender chunks of banana with glass strain and boiled water aloe vera is also taken. When symptoms of CHIKV begin to appear must be combated immediately, since fifteen minutes of receiving the infection process of spreading the infection is triggered and after three hours spreads through blood vessels. Against CHIKV should take four glasses daily for a week by mixing two concoctions: a boiling concoction ginger, lemongrass, pepas of black pepper and lemon peel. When lowering the fire you add lemon juice and honey. The other concoction boiling elderberry sauce or alone is made. Then mix equal parts of both potions and four glasses a day are taken. The active agent CHIKV not stay more than two days. 2. nanotherapies-based treatments with electrical, audio and magnetic frequencies: People affected by the CHIKV can also access treatment with electric waves, provided they do not have implants, prostheses, pacemakers or any metal or synthetic inlay. For a professional in bioinformatics it is known that each infectious agent emits a specific frequency based on the DNA unmistakable. On this basis it is possible to enter the field of nanotechnology and apply electroporation CHIKV DNA to clear his field of electrostatic forces and thus destroy the CHIKV.

The method for removing part CHIKV to know the frequency of emission identifying this pathogen. CHIKV frequency is 570 Hz. To remove it would be necessary to issue you a 6270 Mhz frequency linear and would be removed in 32 minutes. But with a device that emits waves Quadratic be sufficient frequency 1400 MHz for only 2 minutes! If a device that emits waves with parallel Quadratic pulsations in milliseconds, using the 1070Mhz 1080 Mhz frequencies and eliminate CHIKV DNA in just a minute and a half would be used! A wave emitting device and creating audio fields of magnetic poles would also be useful, applying 30 Mhz for 20 minutes. Finally, the use of magnetron also be very effective, since in just five minutes electrostatic fields CHIKV DNA forces would destroy, alter intracellular ionic conditions of the human being infected. * Prof. specialist in biomedicine. Information for Third.

Genital herpes during pregnancy – Blog – embarazada.com


During pregnancy, it is very important that the mother takes into account a number of precautions to ensure you are doing everything in their power to have a healthy and strong baby. Once the mother confirmed her pregnancy or suspect is in a state, you must schedule an appointment prenatal. In that event, the doctor will assess the physical condition of the mother, the baby, the week in which it is located and must perform a series of tests to verify if the mother has or not a condition that endangers the pregnancy, health or the baby. One of the tests that the mother must be done is aimed at verifying the presence of sexually transmitted diseases (STDs) such as gonorrhea, syphilis, chlamydia, trichomoniasis, herpes, etc. Early diagnosis of most STDs prevents the risk that the baby may suffer damage to their health in the short, medium and long term. What is herpes? Genital herpes is a sexually transmitted disease that has become increasingly common in recent years. In many cases, the symptoms of genital herpes are very mild and tend to be confused with skin conditions, so many people who have the disease do not know they are infected. When present, symptoms are: • blisters on the genitals, mouth or rectum • The first time the person has blisters, usually have symptoms like fever, body aches and swollen lymph nodes near How herpes can affect the baby? The risks of having herpes during pregnancy are:

• If the mother has a recurrent infection in pregnancy, the baby is about 1% of contracting the disease • Increased risk of spontaneous abortion • Increased risk of preterm birth • Birth Defects Many doctors prefer that the mother gives birth by caesarean section scheduled for that herpes is not caught the baby, because it could be fatal. The doctor’s decision will vary depending on whether the herpes is active or not at the time of delivery. That is, if at the time of childbirth the mother has blisters on the cervix or in the genital area or any symptoms associated with the disease, the doctor will opt for performing a cesarean section to prevent the baby is in contact with the infection .

symptoms, prevention and remedies, symptoms of cold sores on the lips, home remedies and prevention

Fever blisters are also known as cold sores. Fever blisters are caused by the virus known as herpes simplex. They can last up to ten days. It is a painful condition. Blisters may appear on the gums, lips, around the mouth, nose, cheeks, or fingers. Blisters are contagious until the complete crust is formed. It is not a serious condition. It can cause problems in patients with low immunity or weak. Fever blisters are caused due to infection by the herpes simplex virus that has two types namely HSV 1 and HSV 2. These viruses can cause cold sores around the mouth and lips. When fever blisters occur on the lips, which is called as cold sores. This infection spreads through direct contact with an infected person. If someone is using the same utensils or the razor of an infected person, you can get the infection.

If one or kissing an infected person comes into contact with the saliva of an infected person, then you are at risk of developing an infection. Virus enters the body through the broken around the mouth or lips skin. Symptoms of cold sores on the lips Some of the common symptoms associated with fever blisters are: The bubbles can be seen on the lips and around the mouth. Area around the bubbles appear in red. The bubbles are often painful. Fever and chills. The enlargement of the lymph glands in the neck. After a few days, the blisters open and clear leaking liquid break it. Then form crust. Within fifteen days bubbles disappear. Diagnosis: The diagnosis is made by examining local history and the patient’s physician.

Usually, the test is not necessary. Home remedies and prevention of cold sores Usually, no treatment is needed. Blister disappear within two weeks. Medications may be given to reduce pain. The local application of ointments or creams is considered to reduce the intensity of symptoms. Herpes simplex virus remains dormant in the body once it is infected with it. You can get recurrent attacks of cold sores. The treatment will help reduce the number of attacks. Avoid contact with the infected person. Do not kiss the affected person. Do not share utensils or food the patient. Once the person is infected with herpes simplex virus, you must take certain precautions to reduce the number of attacks.

To improve immunity, you have to take a balanced diet rich in vitamins and minerals. Protein diet will help repair cell damage. Vitamin C keeps you from viral infection. Include citrus fruits such as gooseberry, lemon and orange in your diet. Drink plenty of water. Fever blisters are aggravated by exposure to sunlight. Avoid prolonged exposure to sunlight. Use sunscreen before going out in the sun. If you are suffering from cold sores, do not touch the sores. This will prevent the spread of other body parts. Wash your hands frequently with soap and water. Apply ice bubbles as soon as you notice tingling pain on the lips. You can prevent blistering.

Avoid being stressed. Practice relaxation techniques. Homeopathy can help get rid of herpes infection and prevent recurrence. Local application of pure aloe vera gel can help. The local application of calamine lotion help. If necessary, antiviral drugs can be taken after consulting a doctor.

Is Dangerous Type 1 Herpes? Is there a cure?

The type 1 herpes, also known as herpes simplex or HSV-1 is the most common and at the same time most contagious of all viruses of this knowledge. Its name comes from the Greek meaning “crawl” because of the ability to develop in a short time. In this article I will give some important facts about herpes so you’re cautious and you avoid becoming infected. Or at least you treat you accordingly. Information about type 1 herpes Herpes type 1 is a disease of infectious and viral type is characterized by the appearance of skin lesions or in clusters surrounded by a red circle. While mainly it affects the mouth and lips are cases of people with the herpes simplex virus other body parts such as genitals or face. There are different ways of treatment to cure injuries and reduce symptoms. There are also techniques that help the virus does not manifest again in the future (regrowth). It is worth noting that the first occurrence is very painful blisters that most people have an outbreak again in your life. For that to happen the symptoms become milder. If you go to the doctor at the type 1 herpes sure you indicate treatment with certain drugs such as acyclovir. Let me tell you if it serves to reduce symptoms and speed healing of blisters has no effect to eliminate the virus forever nor prevent regrowth.

This means you’ll spend a good amount of money (not very cheap drugs) only to heal a wound. I always recommend to those who ask me that in that case it is better to opt for home remedies such as aloe vera, essential oil, castor oil, dairy products, among others. To prevent future outbreaks appear, leads healthy habits: Know what the risks are returning to suffer herpes In case you have a weakened immune system, diseases such as HIV or cancer, eczema, you are undergoing chemotherapy, surgery or you have’re convalescing and have severe burns, are more likely to reoccur. Determine the potential triggers Some can not be modified such as hormonal changes or menstruation, but there are others who do. It is the case of stress, fatigue or anxiety. Do not expose yourself to too much sun It is one of the most common triggers of type 1 herpes so I recommend that you get a good factor of protection and proper clothing also not out on the street at noon. Finally, I want to recommend a completely natural and safe to control outbreaks and make these are becoming less frequent and shorter method. It is the ULTIMATE PROTOCOL OF HERPES, Melanie Addington. There you will have all the detail of foods you should include in your diet and what you have to remove if you want to weaken the virus and keep herpes outbreaks under control.

And you also have a list of recommendations and home remedies that will give immediate relief to burning. The best of this step by step guide is that you have a complete and comprehensive plan of action, with amazing benefits for your health. Will help strengthen your immune system and this will create a sort of insurmountable barrier for herpes simplex type 1 virus-and for other diseases too! CLICK HERE NOW to combat herpes from its root with the simplest and most complete method. You may also like:

4 preventive techniques to avoid genital herpes

Is it possible to get rid of genital herpes forever? The sad truth about herpes is that once it infects you, you can carry the virus for life. But carry the virus for life does not have to mean you have herpes symptoms for the rest of your life too. Yes, get rid of herpes in life is possible – well, actually one can not get rid of the virus – but certainly can get rid of the signs and symptoms associated with it. There are many people with herpes who are living their lives the way they want because they have learned to manage their symptoms of herpes. You can get rid of genital herpes by preventing signs and symptoms when they appear. Here are some important points you need to know in order to get rid of the symptoms of permanent genital herpes: 1. Dieta for herpes: follow a strict diet is helpful in managing the symptoms of herpes. There are some foods that will not take, especially those rich in arginine, which can aggravate your herpes symptoms appear and engage each. These foods include nuts, raisins and chocolate. Citrus and processed foods should also be avoided.  2.

Remedios natural herpes: there are plants that act as natural medicines for herpes, such as licorice root and garlic. These two plants have antiviral properties. The use of natural remedies to get rid of genital herpes is more beneficial than the use of powerful drugs that can have side effects too often.  3. Suplementos: Taking supplements of vitamins and minerals along with the anti-herpes specific remedies is also a smart in managing the symptoms of herpes alternative. These supplements can sometimes be a combination of several antiviral ingredients and therefore produccen better effect in managing their symptoms. 4. Homeopathic remedies: the use of homeopathy in the treatment of herpes is effective. I have experienced remarkable results after use. Unfortunately, many homeopathic providers out there just do not seem brands know what they are doing. Or they are trying to turn into a nonexistent homeopathy cure (the virus remains in the body) or the simple sale of so-called combined remedies, which are far from being efficient at a very high price. As today, no cure for herpes known. That is why it is impossible for me to say that you can totally get rid of the genital herpes virus with this treatment regimen, but what can surely eliminate your symptoms.

To control the symptoms of genital herpes, all you have to do is modify your lifestyle and diet. Unless your diet based on junk food and soda or beer every day, it does not have to be too drastic a change. A drastic diet is sometimes necessary only in very specific cases. With reasonable adjustments to diet, lifestyle and supplements you take – you will get rid of genital herpes for the rest of your life. Get your FREE report with the insider secrets of my personal experience on how to remove herpes from your life now! You want a solution that will help you naturally cure herpes symptoms fast? Would you like your herpes outbreaks not return?