Herpes Simplex – Symptoms, Diagnosis, Treatment of Herpes Simplex

Reference from A. D. A. M. Back to TopCauses There are two strains of herpes simplex viruses:  Herpes simplex virus type 1 (HSV-1)  Usually is Associated With infections of the lips, mouth, and face. It is The most common herpes simplex virus and many people Develop it in childhood. Often HSV-1 causes sores (lesions) inside the mouth,: such as cold sores (fever blisters), or infection of the eye (especially the conjunctiva and cornea). It can lead to infection Also of the lining of the brain (meningoencephalitis). It is transmitted by Contact with infected saliva. By adulthood, 30-90% of people will Have antibodies to HSV-1.

The likelihood of childhood infection is higher socioeconomic Among Those With lower status.  Herpes simplex virus 2 (HSV-2)  Usually it is sexually transmitted. Symptoms include genital ulcers or sores. However, some People with HSV-2 have no symptoms. Up to 30% of adults in the U. S. Have antibodies against HSV-2. Cross-infection of type 1 and 2 viruses from May Occur oral-genital contact. That is, you can get genital herpes on your mouth, and oral herpes on your genital area. A finger infection, called herpetic whitlow, is another form of HSV infection. Usually it Affects health care providers are exposed to saliva, WHO During Procedures. Sometimes, young children can get the disease Past.

HSV can infect a fetus and cause abnormalities. A mother Who is infected With transmit the virus HSV May to vaginal delivery During newborn her, Especially if the mother has an active infection at the time of delivery. However, 60 to 80% of HSV infections acquired by newborns Occur in Women Who Do not Have symptoms of HSV infection or a history of genital HSV infection. It’s possible for the virus to be transmitted even When there are no symptoms or visible sores. Two-Thirds of People with genital HSV infection Have Their Recurrences of symptoms, and one-third or more Recurrences Have three (Outbreaks) per year. HSV is never eliminated from the body, but stays dormant and can reactivate, Causing symptoms.

Coated tablets Valtrex

Composition: Each film-coated tablet contains 500 mg of valacyclovir. List of excipients: Core: microcrystalline cellulose; crospovidone; povidone; Magnesium Stearate; Colloidal Silicon Dioxide. Coating: Carnauba Wax; hypromellose; Titanium dioxide; Macrogol 400; Polysorbate 80; 95% ethanol; Propylene glycol; Shellac; FD \x26amp; C Blue No. 1; Sodium Lactate; Polydimethyl siloxane. Therapeutic Action: ATC Code: J05AB11. Indications: Valtrex is indicated for the treatment of acute herpes zoster in immunocompetent adults located. Valtrex is indicated for the treatment of initial and recurrent episodes of genital herpes in immunocompetent adults. Valtrex is indicated for chronic suppression of recurrent episodes of genital herpes in immunocompetent individuals. To reduce the risk of transmission of genital herpes susceptible to heterosexual couples, in combination with safer sex practices. Valtrex is indicated for the prophylaxis of cytomegalovirus infection and disease (CMV) after organ transplant. Valtrex is used to treat cold sores. Properties: Pharmacodynamics: Mechanism of Action Valaciclovir, an antiviral, is the L-valine ester of acyclovir. Acyclovir is a purine nucleoside analogue (guanine).

Valacyclovir is converted rapidly and almost completely in man to aciclovir and valine, probably by the enzyme called valaciclovir hydrolase. Acyclovir is a specific inhibitor of herpesvirus with in vitro activity against herpes simplex virus (HSV) type 1 and type 2, varicella zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV) and human herpes virus 6 (HHV-6). Acyclovir inhibits DNA synthesis herpes virus once it has been phosphorylated to the active triphosphate form. The first stage requires phosphorylation activity of a specific enzyme to the virus. In the case of HVS, VZV and EBV this enzyme is viral thymidine kinase (TK), which is only present in virus-infected cells. Selectivity is maintained in CMV with phosphorylation, at least partially mediated through the phosphotransferase gene product of UL97. This requirement for activation of acyclovir by a virus specific enzyme largely explains its selectivity. The phosphorylation process (conversion from mono to triphosphate) by cellular kinases is completed. Acyclovir triphosphate competitively inhibits viral DNA polymerase and incorporation of nucleoside analogs results must result in chain termination, thus stopping the viral DNA synthesis and therefore blocking virus replication. Pharmacodynamic Effects resistance phenotype usually deficient thymidine kinase is in producing a virus with severe disadvantages in the natural host. Infrequently, it described reduced sensitivity to acyclovir as a result of subtle alterations in thymidine kinase or DNA the viral polymerase. The virulence of these variants resembles that of wild-type virus. Extensive monitoring of clinical samples of HVS and VZV patients on therapy or prophylaxis with acyclovir has revealed that virus with reduced sensitivity to aciclovir is extremely rare in immunocompetent individuals, and are only seen very rarely in individuals severely immunocompromised for eg.

, transplant recipients, organ or bone marrow, patients receiving chemotherapy for malignant disease and people infected with human immunodeficiency virus (HIV). Absorption: After oral administration, valaciclovir is well absorbed and converted quickly and almost completely to acyclovir and valine. Probably, this conversion is mediated by an enzyme isolated from human liver is known as valaciclovir hydrolase. The bioavailability of acyclovir in 1000 mg valaciclovir is 54% and is not reduced by food. Mean aciclovir peak concentrations are 10 to 37 micromoles (2. 2 to 8. 3 micrograms / ml following single doses of 250-2000 mg valaciclovir in healthy subjects with normal renal function, and occur at a median time of 1 to 2 hours post -dosis. peak plasma valacyclovir concentrations are only 4% of the levels of acyclovir, occur to a median time from 30 to 100 min. post dose, and are at or below LOQ 3 hours after dosing . the profiles pharmacokinetics of valaciclovir and aciclovir are similar after single and repeated dose. the herpes zoster and herpes simplex do not significantly alter the pharmacokinetics of valaciclovir and aciclovir after oral administration of valaciclovir. in a pharmacokinetic study of valacyclovir and acyclovir during late pregnancy, the daily ABC steady state acyclovir (area under the plasma concentration curve over time) after 1000 mg valaciclovir was about 2 times higher than that observed with oral acyclovir to 1200 mg daily. In patients with HIV infection, layout features and pharmacokinetics of acyclovir after oral administration of single doses or multiple of 1000 mg or 2000 mg valaciclovir not altered compared to healthy subjects.

In transplant recipients who received valaciclovir 2000 mg four times a day, peak acyclovir concentrations were similar or higher than those in healthy volunteers who received the same dose. ABC estimated daily are significantly higher. Distribution: Binding of valaciclovir to plasma proteins is very low (15%). Elimination In patients with normal renal function, the plasma elimination half-life of acyclovir after single and multiple doses of valaciclovir is approximately 3 hours. In patients with end-stage renal disease, the average elimination half-life of acyclovir after valaciclovir administration is approximately 14 hours. Less than 1% of the administered dose of valaciclovir is recovered in urine as unchanged drug. Valaciclovir is eliminated in urine mainly as acyclovir (more than 80% of the recovered dose) and metabolite known acyclovir, 9- (carboxymethoxy) methylguanine (CMMG). Preclinical Safety Data: The results of tests in vitro and in vivo mutagenicity indicate that Valtrex is unlikely to cause a genetic risk in humans. Valaciclovir was not carcinogenic in bioassays conducted in mouse and rat. Valaciclovir did not affect fertility in male or female rats receiving oral dosing. Valaciclovir was not teratogenic in rats or rabbits. Valacyclovir is metabolized almost entirely to acyclovir. Subcutaneous administration of aciclovir in internationally accepted tests did not cause teratogenic effects in rat or rabbit.

In additional studies in rat fetal abnormalities at subcutaneous doses that produced plasma levels of 100 micrograms / ml and maternal toxicity. Dosage: Adults: Treatment of herpes zoster: The dosage is 1000 mg of Valtrex to be taken 3 times a day for 7 days. Treatment of genital herpes simplex infections: The dose is 500 mg of Valtrex to be taken 2 times a day. For recurrent episodes, treatment should be for 5 days. For initial episodes, which can be more severe, treatment may have to be extended to 10 days. Dosing should begin as soon as possible. For recurrent episodes of herpes simplex, ideally this is done in the prodromal or as soon as the first signs or symptoms appear period. Prevention (deletion) relapse of genital herpes simplex infections: In immunocompetent patients taking 500 mg of Valtrex 1 time a day. Some patients with very frequent recurrences (eg 10 or more per year) may benefit more when the daily dose of 500 mg is taken in divided form (250 mg two times a day). Reduction of transmission of genital herpes: In immunocompetent heterosexual adult with 9 or fewer recurrences per year, the infected partner should take Valtrex 500 mg 1 time a day. No data on the reduction of transmission in other patient populations. Prophylaxis against infection and disease by cytomegalovirus (CMV): Dosage in adults and adolescents (from 12 years of age): The dosage of Valtrex is 2 g 4 times a day and after the transplant should begin as soon as possible. This dose should be reduced according to creatinine clearance (see below Dosage in renal failure).

The duration of treatment will usually be 90 days, but may need to be extended in high risk patients. Cold Sores: 2 g 2 times a day for one day is effective treatment. The second dose should be taken about 12 hours after the first dose. When this dosage regimen is followed, the treatment should not exceed one day, as it has been shown that this does not provide additional clinical benefits. Therapy should be started from the first signs of an outbreak of cold sores (eg. , Tingling, itching or burning sensation). Children: No data are available on the use of Valtrex in children. Elderly: The possibility of renal impairment in the elderly should be taken into account to adjust the dose as needed. It is necessary to maintain proper hydration. Renal impairment: Caution should be exercised when administering valaciclovir to patients with kidney function affected. Adequate hydration should be maintained. Treatment of herpes zoster, prevention (suppression) of herpes simplex and reducing transmission: The dosage of Valtrex should be reduced in patients with impaired renal function significantly affected, as shown in the following table: See Table In patients undergoing hemodialysis, should be used Valtrex dosage recommended for patients with a creatinine clearance below 15 ml / min. This should be administered after hemodialysis has been performed.

Prophylaxis against CMV: The dosage of Valtrex should be adjusted in patients with renal insufficiency, as shown in the following table: See Table Creatinine clearance should be monitored frequently, especially during periods when renal function is changing rapidly; for example, immediately after transplantation or engraftment. Valtrex dosage should be adjusted in accordance with the above. Dosage in hepatic impairment: Studies with a 1 g unit dose of Valtrex show that it is not necessary to modify the dose in patients with mild or moderate cirrhosis (hepatic synthetic function maintained). The pharmacokinetic data in patients with advanced cirrhosis (liver failure in synthetic function and evidence of systemic-site shunting) do not indicate the need for dose adjustment; however, clinical experience is limited. For higher doses (4 g or more / day), see Warnings. Side effects: Adverse reactions are listed below by system organ class and according to the Medical Dictionary of Regulatory Activities (Medical Dictionary for Regulatory Activities [MedDRA]) and frequency. The frequency categories used are: Very common: ³ 1 in 10. Common: ³ 1 in 100 and

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ࡱ> HJ G [@ % bjbj44 .>ViVi ˆ bbbbvL s $sR j- -ppp V p pHp ::, — š b:”f C0sp ./ \\ // PDBF b INCLUDEPICTURE “http://www.sefh.es/gefp1/images/Image1.gif” \\ * MERGEFORMATINET Canario Service of the University SaludHospital Maternal InfantilLas Palmas de Gran CanariaINFORME fOR CFyT. Author: Dobrito A; November 2004 generic name: valaciclovir Requested by: Dr. Blanco-Soler (Gynecology Service) Application Date: 18/08/2004 Trade name: various specialties (ValherpesValtrex, Virval) Group terap utico: J05AB: Antivirals: nuclesidos and nucletidos except reverse transcriptase inhibitors. Commercial presentation: tablets 500 mg and 1 g. teraputicas Indications: prevention and treatment of Herpes zoster treatment of recurrent herpes simplex infections Posologa: Adults: Herpes Zoster: 1 g / 8h for 7 days, starting treatment within 72 hours after the appearance No lesions. Herpes simplex: initial episodes, 500 mg / 12 h for 10 days. For recurrent episodes, 500 mg / 12 h for 5 days, starting treatment during the prodromal period or when the first symptoms appear. Prophylaxis of Herpes simplex infections: in immunocompetent patients, 500 mg / 24 h to 500 mg / 12 h in immunocompromised patients. For frequent recurrences (10 ms per year) 250 mg / 12 h. In patients with renal insufficiency, a dose adjustment in function of the degree of impairment if necessary. In case of mild to moderate cirrhosis it is not necessary to adjust the dose. In case of advanced cirrhosis, in principle you do not need dosage adjustment, although the data are limited clnicos. Mechanism of action: profrmaco of acyclovir, hydrolyzed form quickly and almost completely to acyclovir and valine by the enzyme valacyclovir hydrolase. Acyclovir has virosttica action; act by inhibiting cell synthesis of viral DNA, after fosforilacin in cells infected by the virus to its active triphosphate form. The need for activation of acyclovir by a viral enzyme, explains its selectivity. Spectrum of activity: acyclovir act exclusively on DNA viruses, especially Herpes simplex types 1 and 2, varicella-zoster virus, cytomegalovirus, Epstein-Barr virus and human herpes virus 6 farmacocintico Profile: after oral administrcin valacyclovir is rapidly absorbed and independently of the presence of food. The daily acyclovir AUC after administration of 1 g of valacyclovir three times a day is 2 times higher than expected with oral acyclovir 800 mg 5 times a day. Elimination half-life of acyclovir after plasmtica a unique and mltiple dose valaciclovir is 3 h approximately. Less than 1% of the administered dose of unchanged valaciclovir is recovered in urine. Valaciclovir is mainly eliminated in urine as acyclovir and its metabolite 9-carboxy-methoxymethyl-guanine. Adverse effects: gastrointestinal complaints have been described as nausea, abdominal pain, vomiting and diarrhea; exantemticas headaches and rashes including photosensitivity reactions, urticaria or pruritus. In rare cases they have appeared thrombocytopenia, dyspnea, angioedema and anaphylaxis, renal insufficiency, increase in transaminases and neurolgicas hepticas disturbances such as dizziness, confusion, hallucinations, loss of consciousness and very rarely eat. In severely immunocompromised patients, prolonged treatment with valaciclovir, there are reports of renal failure, hemolytic anemia and thrombocytopenia microangioptica. clinic and comparative efficacy with other antivirals: valacyclovir compared with acyclovir has been in several clnicos trials, although they will present the results of a multicntrico, randomized, double-blind. Beutner et al compared in 1147 patients the results of efficacy, safety and plasmticos acyclovir levels in 3 groups of patients: group 1 (valaciclovir 1 g / 8 h for 7 days), group 2 (valaciclovir 1 g / 8h for 14 das) and group 3 (acyclovir 800 mg 5 times a day for 7 days) for the treatment of herpes zoster. The variables studied were: t necessary for removal of pain, t until the cessation of appearance of new lesions and / or increase the area of ​​the lesin; t cicatrizacin of injuries; plasmticas concentrations of acyclovir the days 3, 7 and 14 and secondary variables such as pain intensity or quemazn, utilization of painkillers … The pain REMITI before groups with valaciclovir ( 38 and 44 days for treatments 7 and 14 days) with acyclovir (55 days; p = 0.001 and p = 0.03, respectively). The number of patients still in pain at the end of the study was slightly higher in groups with acyclovir (19.9% ​​for group 1, 18.6% for group 2 and 25.7% for the group of acyclovir ; p = 0.02). The postherptica neuralgia appeared in 79% of patients in group 1, 80% in group 2 and 85% of the group of acyclovir. The adverse event profile was similar in the 3 groups. The majority of adverse effects were mild-moderate character. The most common were nausea and vomiting with 2 frmacos (25% of patients in group 1, 21% in group 2 and 27% of group 3). There was only 1 case of severe headache treatment with valaciclovir. There were no statistically significant changes in biochemical parameters and hematolgicos in any of the 3 groups. The plasmticas concentrations were higher in the groups of valaciclovir in group 3; the estimated after administration of valacyclovir the AUC was 393 (versus 178 M.h (M.h in the case of acyclovir.

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Chickenpox – Diseases – ZonaMedica.com.ar

Chickenpox: Description It is one of the most common infectious disease of childhood and is caused by a herpes virus group called Varicella -Zoster, which causes a particular rash, accompanied by severe itching, which manifests with small clustered, flat or embossed spots, blisters liquid and scabs and fever. It is one of the diseases that are transmitted more easily and therefore is highly contagious. While severe complications related to chickenpox are rare in children with normal defenses (immunocompetent) and usually does not pose a threat to the life of healthy children, the disease is most dangerous in infants, immunocompromised patients and the grown ups. When a teenager or an adult chickenpox is contagious, the disease course will be longer and more severe and can develop pneumonia. The most common complication of chickenpox is the skin infection by bacteria. It can also complicate or viral encephalitis or bacterial pneumonia. Causes of Chickenpox The virus spreads easily from person to person via aerosolized droplets from coughing or sneezing and airborne. It can also be transmitted by contact with infected or by direct contact with the blisters of the skin tissues. Transmission can occur from the first symptoms and until all blisters have crusted over like, so the isolation of sick of other people who have not had the disease is recommended. Varicella zoster virus remains dormant in the body but can reactivate, causing shingles, another type of rash that manifests in blisters with fluid and is very painful. Chickenpox generally results in lifelong immunity.

Symptoms of Chickenpox The period between the first contact with the virus and the appearance of symptoms varies between 9-21 days. It manifests with headache, fever and general malaise, which may be accompanied by nausea, vomiting and chills. But undoubtedly the most characteristic sign is the outbreak with vesicles or blisters all over the skin: hair, leather and even genital lesions appear in the mouth, which is then manifested in 24 or 36 hours, characterized by intense itching. This process extends to approximately the sixth day. The blisters burst releasing a (highly contagious) clear liquid and after 4 to 5 days scabs Thereafter begin to diminish spots and scabs disappear completely on the twentieth day about form. They can produce sores if they appear in the mouth, eyelids, rectum, vagina and upper respiratory tract. Diagnosis of Chickenpox The type of rash and symptoms are so characteristic that the doctor easily diagnosed. Important The symptoms described here concerning this disease can be confused with other diseases. To establish a proper diagnosis, always consult your doctor. The objective is to inform and educate MédicosExpertos, so descriptions of diseases here brindadas not replace a professional consultation. illustrative image

Italian translator of Varicella

 Varicella English chickenpox, varicella Dictionary source: Babylon Italian-English dictionary More: Italian to English translator More Languages: [top]  Varicella in Italian Chickenpox, sing. VARICÈLI / E, pl. Varicella, infettiva malattia dell’ìinfanzia di origine virale che si e manifest with febbre vescicole sulla pelle.

SQUACIARÓLA, sing. SQUARCIRÓLI / E, pl. , Varicella. , VAROLI, heal lasciata dalla antivaiolosa vaccinazione, abolito ora è stato method tale. More: Translator Italian to Italian The varicella ed è a highly contagious Epidemica causata esantematica malattia da il un’infezione primary with varicella-zoster virus (VZV or umano Herpesvirus 3), a DNA virus Herpesviridae appartenente alla famiglia, sottofamiglia Alphaherpesvirinae, generate Varicellovirus. The condizione inizia vescicolare solitamente with cutaneous rash, mainly esteso the corpo e alla testa or anche alle estremità. Le vescicole guariscono poi lasciare senza cicatrici. All’esame, l’Osservatore trova in genere lesioni in vari Stadi di guarigione.

Per saperne di più visit Wikipedia. org . . . Copyright: © Questo articolo tratto utilizza materiale dell’Enciclopedia online Wikipedia® ed è sotto la licenza autorizzato GFDL More: Translator Italian to Italian  Varicella in Russian (F) ветрянка source dictionary: Italian – Russian (AK) More: Italian to Russian translator  Varicella in Bulgarian f варицела. Dictionary source: Bulgarian Italian dictionary More: Italian to Bulgarian translator

 Varicella in Bosnian male boginje source dictionary Bosnian Italian dictionary More: Italian to Bosnian translator  Varicella in Portuguese chickenpox source Dictionary Portuguese Italian Dictionary More: Translation from Italian to Portuguese  Varicella in Albanais n. likardhë, lingardhë, li and dhenve. source dictionary: Albanian Italian dictionary More: Translator Italian to Albanais

 Varicella in German Windpocken Dictionary source: ADO’s Dictionary Italian German More: Translation from Italian to German  Varicella English chickenpox source Dictionary Italian-English Online More: Italian to English translator  Varicella in Interlingual n sf varicella source Dictionary Italian Dictionary Interlingua More: Translator Italian to Interlingual  Varicella in Finnish

vesirokko source Dictionary Italian-Finnish Dictionary More: Translation from Italian to Finnish  Varicella in Spanish F. chickenpox source Dictionary Spanish Italian Dictionary (GI) More: Italian to Spanish Translator

Herpes simplex type 1 virus particle, computer illustration. HSV …

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The causes of a swollen lip / radikewl

Other people are reading What are the causes of a swollen lip. lip image by KWAP from Fotolia. com Lip swelling Swelling of the lips can be caused by many different factors, which include allergic reactions and medical conditions. You know what foods to avoid and what allergens that contribute to inflammation are; which also keep you informed about the type of medical conditions that contribute to make your lips swell, it can also be an important first step in your treatment. allergic reactions Allergic reactions to certain foods, medications and environmental conditions may cause the lips to swell. Many cases of swollen lips are caused by food allergies, which occurs when the immune system attacks a food that has entered the body. A tingling sensation or tingling around the mouth or, as first tongue or throat, can occur as a reaction. This can be followed by an inflammation in the mouth. Symptoms such as these can occur a few minutes after eating the food.

The best way to treat inflammation in the mouth, in these circumstances, is to deal first allergen. This may mean taking an antihistamine or prescribed medication without a prescription such as Benadryl, which should reduce or completely eliminate swelling on the lips. other causes There are many diseases that can also contribute to swollen lips, including herpes simplex or swelling of the lips due to cheilitis. Herpes simplex virus, also known as cold sores, can be caused by stress, colds, flus and any changes in the immune system. A side effect of the virus could be an ulcer in the mouth, which could also be accompanied by inflammation around the lip area. Swelling of the lips can also be caused by a cheilitis. Cheilitis is inflammation of the mouth caused by different factors, such as atopic dermatitis. Editor’s pick Ten rules about weight loss you should follow You may also like . . .

2014-Family Herpesviridae

family Herpesviridae General characteristics to all members of the Family CityReporters in Subfamilies Herpes Simplex Virus Type 1 (HSV-1) Mechanisms of Evolution ICTV: International Committee on Taxonomy of Viruses Order: Herpesvirales Family Alloherpesviridae (fish and amphibians) Family Herpesviridae (herpes virus of mammals, birds and reptiles) Family Malacoherpesviridae (bivalves) A typical herpes virion Core

with double-stranded linear DNA (from 124 to 295 kb) capsid icosahedral (161 capsomeres + 1 capsomeric structure for packaging and release of the genome) integument: amorphous material appearance Envelope : With viral glycoproteins (spicules) Distribution in nature Is it so highly disseminated in nature It is likely that their number exceeds the more than 200 identified to date Most animal species have had at least one herpesvirus herpesvirus

Herpes Simplex Virus 1 (HSV-1) Herpes Simplex Virus 2 (HSV-2) Human Cytomegalovirus (HCMV) Varizella-Zoster Virus (VZV) Epstein-Barr Virus (EBV) Human Herpesvirus 6A, 6B and 7 (HHV-6A, 6B, 7) 4 overall biological properties 1: Encode a large number of enzymes involved in: -He nucleic acid metabolism (Eg thymidine kinase, dUTPasas, among others) – DNA synthesis

(DNA pol, helicases, primases) -He processing of proteins (Protein kinases) 2: viral gene transcription , DNA synthesis and the nucleocapsid assembly occur in the CORE 3: Production of progeny viral infectivity involves the destruction of the infected cell

replication lytic cycle 4: They are able to stay latent in its natural host and then recover Latent infection episomal viral genome with a limited expression of specific maintenance dormancy (transcribed LAT) and without producing infectious viral particles genes (not Inf. Chronicle) viral strategy to evade detection by the immune system Under certain conditions STATE TAKEOVER Infective with the consequent production of new infectious viral particles that initiate clinical recurrence

There are differences between family members: In the range of host At the time of replicative cycle In the cell in which remain dormant In the clinical manifestations that cause Biological properties 70′ Alpha-herpesvirinae Beta-herpesvirinae Gamma-herpesvirinae They are neurotropic (infected tissues Nervous System) relatively short replicative cycle (~ 18 hrs) efficient destruction of infected cells Range variable hospedero

Rapid spread in culture Latency: mainly in sensory ganglia HSV-1 HSV-2 VZV Reduced host range long reproductive cycle (approximately 7 days) Slow progression in culture Infected cells (cytomegalovirus) enlarge Latency: secreting glands, lymphoreticular cells, kidneys and other tissues Some may develop auditory, visual, neurological problems. Sometimes premature labor, small for gestational age, jaundice, liver and spleen thickened, microcephaly, seizures, and difficulty eating erupsiones In immunocompetent:

Symptoms similar to those of mononucleosis In immunocompromised patients: Serious infections CMV HHV 6 and 7 Roseola Lymphotropic: specific B and T cells Latency: lymphoid tissue EBV In some patients it is associated with Multiple Sclerosis chronic inflammatory CNS disease where cells attack the myelin surrounding axons of nerve cells Epstein-Barr Virus Might Kick-Start Multiple Sclerosis. Science News, 2006 taxonomy:

Order: Herpesvirales Family: Herpesviridae Subfamily: Alpha-herpesvirinae Genre: Simplexvirus natural host: tropism: primary site of infection: mucosal epithelial cells lytic replication latent phase: in sensory neurons (ganglion) Distribution: Worldwide Transmission: contact, saliva Infects approx. 90% of the adult population

Virion structure Integument: at least 18 viral proteins. The most important is the virion protein VP16 transactivator also called alpha-TIF YOUR GENOME: linear double-stranded DNA Size: approx 150kpb Covalently linked to in two components: L (long) and S (short) Each component consists of a unique sequence flanked by inverted repeat (ab, b’a’c ‘, ca) the sequence “a” is highly conserved, what varies is the number appearing in such repeated The initial site of infection is oral mucosa, corneal epithelium or skin wounds, where viral replication causes injuries HSV travels by retrograde axonal transport to the sensory ganglion where it establishes latency Under certain conditions HSV reaches the CNS via neuronal probablmente Reactivation: anterograde axonal transport of new progeny HSV to the initial site of infection.

injuries and possible transfer manifest. Virus replication cycle Also endocytosed ENTRY GAG Entry Mediator Herpes Virus FUSION IRREVERSIBLE CORE structural reorganization 6 PROTEINS: ICP0, 4, 22, 27, 47 and US1. 5 Inhibit cellular transcription and promote expression (4-8hrs PI) beta genes Proteins involved in DNA replication (DNA pol) and nucleotide metabolism (Tyrosine kinases) (5-7hrs PI)

Viral DNA replication: A number of proteins are re-beta localizes in the nucleus They are assembled with DNA pre-replicative complex forming) replication Theta Rolling Circle Replication Switch head-tail molecules concatenated cellular factors? Binding protein Source In monomeric molecules are cleaved during packaging model double or single wrap Latent infection Episoma associated with nucleosomes

alpha-TIF The viral genes are inhibited IE Strategy: the viral genome endure and continue living cell To avoid apoptosis or immune response, HSV restricts the expression of their genes to transcript LAT only LAT encodes a miRNA that suppresses the expression of viral proteins IE PI3K activation and Akt pathways by nerve growth factor (NGF) is also favorable to keep the in vitro Latency Nature (2008) 454, 780-783 IE genes DNA replication Under stress conditions: UV exposure emotional stress alteration of hormonal balance

Depression Immune System Among others. . de novo expression of VP16 which is recruited into the nucleus and activates gene expression is induced IE Penkert \x26amp; Kalejta Herpesviridae 2011 2: 3 The reactivation may be asymptomatic or result in recurrent lesions. In immunocompromised individuals can become severe and debilitating injuries HSV property to invade the CNS may result in severe neurological diseases with wear, such as HSV encephalitis antiviral therapy Acyclovir Valacyclovir (prodrug of Acyclovir) Famicyclovir (prodrug Peniciclovir) Valacyclovir and Famicyclovir have better pharmacokinetics

tablet cream cream, pills, intravenously mutations : May occur as a function of error rates of viral DNA pol or the pool and consequently the concentration of intracellular nucleotide precursors recombination intraspecies : It allows a relatively rapid exchange of information within the lineage of the virus. It requires co-infection in the same cell. There is abundant evidence of the use of this mechanism by HSV gene duplication and divergence : Beta-herpesviruses have exploited this mechanism extensively. HCMV encodes five additional families of genes each having from 2 to 12 duplications gene Its use in Gene Therapy

His ability to invade and generate non-toxic latent infection in sensory ganglia neurons and can express transgenes for a long time and actively Genetic complexity of the viral genome can generate many different types of attenuated vectors oncolytic activity with High transgenic ability of the viral particle that allows carry long foreign DNA sequences They are good candidates as vectors for gene transfer because: (Inf. No abortifacient) QUESTIONS? ? Thank you very much Lic. Sabrina Fischer nucleocapsid primary host

Long-term persistence Before the nucleotídocas conocerce and amino acid sequences 30 virion polypeptides (VP) known + 10 virion proteins unconfirmed + Several host proteins at least 11 proteins on the surface, and at least 10 are glycosylated equimolar concentrations of the four isomers Molecular Virology Course 2014

The human papilloma can be cured if detected in time

The human papillomavirus has no cure and is a process which in turn contributes to the care of other sexually transmitted infections.  When a person acquires HPV probably the site where it was purchased, he could also be some other bacteria or viruses that are transmitted this way. The human papilloma virus has no cure, however, is very common to see people with HPV and Herpes, gonorrhea and HPV people finally can coexist some of the microorganisms. HPV also known as the human papilloma virus is transmitted not only through sex there are some strains that are affecting the skin. The lesions are characterized by a kind of warts that can be single or multiple and when placed at the level of the mucosa cause pain, bleeding can sometimes have, also cause of itching are formed. Today it is already possible: the human papilloma can be cured The human papilloma can be cured if detected in time; however, it was very frequents years ago that going to a doctor to have an injury in the genital area male or female, what the doctor always said that many doctors today still maintain is: – We can remove the wart well with trichloroacetic acid, electrocautery, laser cold. but the virus that caused the disease remained living with you for the rest of your life. – The virus will not disappear from your body and warts whenever you are worried appear. – You have to learn to live with the virus, if their defenses down the virus reappears. This was true years ago and is still defending the novelty that some doctors. However, thanks to advances in technology, people have more access to information and today happens that people with this disease have a new option: the possibility of opting for a treatment that tells you that cures the disease.

The human papilloma can be cured if detected in time If a doctor indicated that you are infected with the human papilloma virus, there are behaviors that are not conducive to cure the disease. Including these: – More than one partner without a condom. – Do not know if your partner is healthy or have HPV. Very often people do not talk about their sexual health before going to an intimate act. But I ask you to reflect. If you have HPV and you’ll be intimate with a person if she or he has HPV know what happens: you’ll convey more HPV to your body. – You must not neglect the power as this lowers your immune system and promotes strong and resilient by HPV. – You must not remove the wart with a scalpel. – Being intimate with someone without protection and with the light off you can not see your -anal genital area and legs. Remember that while this wart is no chance of transmission of the virus so dark sexual practices increase the risk of being infected by this virus. If you have had HPV, you have eliminated the warts but you made any of the practices I listed you before, you’re putting at risk of infection by a new species while, you have not given time for the kind of your body is completely eliminated.

That’s why once you remove the wart must meet a step by step treatment that is giving you the guarantee of a cure. Treatment that you can find in the book in PDF Manuel Alfonso Lucas called Sin warts and moles. He is an expert dermatologist as well as natural and holistic medicine. In this book you can download very easily, gives you the guarantee that the natural system implemented step by step cure your disease in a security of 100%. The treatment allows you offer and says that the human papilloma cure, is implemented by yourself at home following the instructions given in a very clear way and are just 5 steps you have to apply. Decide to download here already, you cure HPV.

Herpes infection – Herpes Cure And Treatment

Genital herpes is a sexually transmitted disease, including contagion can occur with oral sex or from mother to child during birth. You can bring as previous symptom and during the appearance of blisters some sort of flu-like. Genital herpes: CDC Fact Sheet. Herpes is a sexually transmitted disease (STD) that any sexually active can get. You can protect against the spread of herpes if: Herpes is caused by a virus: herpes simplex virus (HSV, for its acronym in English). Herpes labialis Posted in Contagion herpes Tags: cause of herpes, herpes infection, herpes contagious, causes cold sores, herpes transmission. Herpes is an infection caused by a herpes simplex virus (HSV). Oral herpes causes sores around the mouth or face. Genital herpes is a sexually transmitted disease (STD). It can affect the genitals, buttocks or anal area. Condoms are the best way to protect against the spread of genital herpes during sexual activity.

Know who they are the most prone to the spread of genital herpes. A specialist will explain the characteristics of genital herpes. A study detailing the people who are most vulnerable to the spread of genital herpes. Discover shingles or herpes on zster, everything about your infection, treatment, symptoms and medical conditions to occur in the body. Herpes is a localized infection, produced by the virus Varicella Zoster, the same that causes chickenpox. Shingles occurs only in people who have already had chickenpox and corresponds to a reactivation of latent virus of the disease. If you want to avoid herpes, it is necessary to prevent the spread of chickenpox. There is now a vaccine against chickenpox and is expected to vaccinees have lower chances of getting herpes ms later. Herpes Simplex – In From 3 to 14 das after the spread of herpes, blisters usually appear in areas such as the mouth, genitals and anus. Days later, these blisters break and a pequeas ulcers appear in infected areas. Many people do not relate the words Herpes Contagion and do not follow protocols to prevent herpes is caught very easily. It also called cold sores and fever, it is presented as a lulcera, which is nothing more than an infection on the lips, mouth or gums DULY.