Medical Microbiology and Parasitology. Volume II: Section V. Virus: Chapter 61. Herpesvirus: Herpes 6

HSV Eraser Protocol
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Available book full text in pdf version The rest of the parts of the book are also available in that format. If necessary you can download the product from Adobe “Acrobat Reader” to display the contents of the book in pdf format by accessing the following link: herpesvirus 6 Herpes 6 virus is the sixth member of the family of human herpesvirus and was first isolated in the laboratory of Robert Gallo at the National Cancer Institute in Bethesda, Maryland, USA, patients with a variety of lymphoproliferative disorders herpesvirus 6 . The human herpesvirus 6 is the sixth member of the family of human herpes virus was isolated for the first time, in 1986, in the laboratory of Robert Gallo at the National Cancer Institute in Maryland, USA from blood lymphocytes peripheral patients with a variety of lymphoproliferative disorders. The isolated virus was a lymphotropic and well distinguishable genetic and antigenic characteristics that differentiate it from all allowed herpesvirus hitherto isolated and placed in the subfamily b herpesvirinae virus. Properties virus The HHV6 genome DNA has a double-stranded, linear, with a size of 155-170 kbp and varies between different isolates. More recent studies, however, have revealed that the HHV6 is more closely related to CMV. It has been shown by analysis of the nucleotide sequence exists 66% sequence homology with CMV. It has been demonstrated by molecular biology techniques the existence of two virus variants: Variant A and B. Both differ in terms of biological, genetic and restriction patterns properties.

Most patients with sudden rash and like febrile illness seem to have HHV6 variant B. HHV6 isolates immunocompromised adult may belong to either variants and at least one patient found both virus variants. The virus has been isolated from peripheral blood mononuclear cells of patients with sudden rash, immunocompromised patients and healthy individuals. It has also been isolated with high frequency from the saliva of HIV-infected patients. The virus replicates in vitro preferably fetal or adult origin phytohemagglutinin-stimulated T lymphocytes. In infected cells they can be detected viral capsids at day 3 and mature virions after 5 days. Pathogeny The main target cell HHV6 appear to be CD4 + lymphocytes. Macrophages are persistently infected and may be an important reservoir. Transformed B lymphocytes, natural killer, megakaryocytes, glial cells, fibroblasts and epithelial cells are able to support the replication of certain strains of virus. Frequent isolations saliva herpesvirus 6 suggest that the virus resides and is removed from the salivary glands. The viral DNA and antigens have been identified in epithelial cells of the salivary glands and from different regions of the upper respiratory tract. So far it is assumed that herpesvirus 6 infection is transmitted by horizontal transmission, and there is no evidence of vertical transmission.

It has been suggested that the Herpes 6 can persist in monocytes / macrophages in a dormant state, although these are not exclusive primary site in vivo latency. The exact mechanism of reactivation of herpes 6 is not clear yet. It has been shown, however, that various types of transactivation can occur between herpes virus 6 and others including CMV, EBV, measles virus and HIV. Is a lymphotropic virus that infects susceptible individuals during the first year of life and generally cause lifelong latency. In a percentage variable, primary infection is followed by an acute illness of short duration, sudden rash. Older individuals may suffer an illness similar to mononucleosis or Kikuchi-Fujimoto disease. It is also capable of causing a wide range of hematopoietic, lymphoid and autoimmune disorders which have been associated with high titers of antibodies to herpes virus 6 and of which the virus has been isolated. These diseases include atypical polyclonal lymphoproliferation of Hogkin disease, chronic fatigue syndrome and systemic lupus erythematosus. General characteristics The herpesvirus 6 virus is ubiquitous in the human population. Infection occurs within the first two years of life; occasionally it is resulting in an acute febrile illness with or without sudden rash. Maternal antibodies are generally present at birth and decline in the first months of life. Seroconversion occurs in most cases between 6 and 18 months and the titles are high in adolescents.

Frequent isolations herpesvirus 6 of saliva suggests that the virus resides and is eliminated from the salivary glands. The viral DNA and antigens were identified in epithelial cells of the salivary glands and from different regions of the upper respiratory tract. So far it is assumed that herpesvirus 6 infection is transmitted by horizontal transmission and there is no evidence of vertical transmission. The most significant property of herpesviruses is their ability to produce a latent infection. During the acute phase of the disease, herpes DNA has been detected in 6 CD4 lymphocytes. During the convalescent phase of exanthem subitum 1. 5 to 2. 5 months after the onset of disease viral DNA is present in a population of adherent cells (monocytes), but not in lymphocytes. It has been suggested that the herpesvirus 6 may persist in monocytes / macrophages in a dormant state, although these are not exclusive primary site in vivo latency. The exact mechanism of reactivation of herpes 6 is not clear yet. Reactivation of the virus seems to occur spontaneously with other herpesviruses in the 5 to 20% of clinically asymptomatic population. It has been shown, however, that various types of transactivation can occur between herpes virus 6 and others including CMV, EBV, measles virus and HIV. clinical data


A variety of clinical disorders have been described as that may be associated with herpes infection 6. Based on current knowledge, which have been insufficient, diseases associated with herpes infection 6 have been classified into 2 groups: diseases caused by herpesvirus 6 infection and disease possibly associated with herpes 6, but without etiologic relationship clearly identified. The first group includes the sudden rash and child-like febrile illness with or without rash, infectious mononucleosis in the absence of heterophile antibodies and cases of Kikuchi disease. The second group consists of certain autoimmune disorders, chronic fatigue syndrome and lymphoid hematopoietic and proliferative diseases. In addition, they have been reported cases of fulminant hepatitis in immunocompromised patients and has been associated with reactivation of herpesvirus 6 and retinitis interstitial pneumonitis. Sudden rash. It is an acute disease that affects mainly small and young adults and is characterized by a short period of high fever (1-5 days) and the appearance of a rash which coincides with the period of defervescence usually occurs in summer and affects both sexes equally. It may be accompanied by sore throat and runny nose. There is absolute neutropenia with lymphocytosis of up to 90% and presence of atypical lymphoid cells with a plasmacytoid cytoplasm. The prognosis is good and does not require treatment. Other febrile illnesses. The virus has been isolated from children with acute febrile disease and otitis and in a percentage of cases the rash may be present. Other symptoms include malaise, irritability, nasal congestion, diarrhea, cough, vomiting.

The picture is benign and does not last more than 4 days. Infectious mononucleosis heterophile absence of Acs. It occurs frequently as a result of reactivation of latent infection by HHV6. The age of patients is the same as those with EBV mononucleosis. It is characterized by an indistinguishable exudative pharyngitis or membranous classical mononucleosis. Lymphadenopathy unlike the MI by the VEB, which tend to resolve in 11 days, may be present to more than 30 days and be associated with hepatosplenomegaly, lymphadenopathy retroperitoneal and blurred vision. Kikuchi disease: This is a histiocytic necrotizing lymphadenitis that has been recently reported. Reported cases come from Japan, Europe, the United States and other parts of Asia. Patients have not painful lymphadenopathy in neck and may or may not be accompanied by sore throat, fever, chills and myalgia. The age of patients ranges between 10and 60 years, with a predominance in 20. Other possible locations of the lymph nodes are axillary, and supraclavicular brachial region. Lymphadenopathy persist for months and can move on to a phase of chronic fibrosis. The prognosis with or without symptomatic treatment is good.

Transplant recipients. Virus reactivation in transplant recipients can lead to interstitial pneumonitis, encephalitis and rejection in some cases. Chronic fatigue syndrome. abruptly starts with a like syndrome accompanied influenza respiratory symptoms and / or gastrointestinal, fever, myalgia, arthralgia, fever, sore throat, unexplained general muscle weakness, excessive fatigue and prolonged postejercicios, neuropsychological symptoms, sleep disorders, among others. These are presented in various combinations, and due to variability among individuals, often the diagnosis of this syndrome is a problem for most doctors. Sjogren’s syndrome. It is an autoimmune disorder characterized by chronic inflammation with infiltration of exocrine glands that can progress to malignant lymphoma. The disease can occur in a primary form, without being associated with connective tissue disease or a secondary form attached artriris rheumatoid, systemic lupus erythematosus or other connective tissue disease. The characteristic and high diagnostic value triad is keratoconjunctivitis, xerostomia and polyarthritis. Any combination of these symptoms can be used for diagnosis. Immunological disturbances consist of functional defects, hyperactivity of B cells and natural killer deficient cells T cells. They can detect a variety of autoantibodies. Systemic lupus erythematosus.

The etiology of this disease is unknown and considered to be a viral infection, altered immune reactivity and genetic predisposition are responsible for the onset of disease. Many infectious agents, they can be imputed to cofactors in disease pathogenesis and herpesviruses are among them. Serological studies have shown high antibody titers against HHV6 in patients with systemic lupus erythematosus. Furthermore they have been detected in biopsy specimens of skin infected with the virus and in primary cultures of peripheral blood lymphocytes of these patients CD4 + / CD38 + was detected the virus genome by in situ hybridization and Acs by immunofluorescence. HHV6 and AIDS. Numerous virus isolates have been conducted in patients with AIDS. Because both viruses share target cell CD4 + lymphocytes, it is suggested that HHV6 is an important step in the progression to AIDS stage cofactor. This virus can cause retinitis in these patients. atypical lymphoproliferative disorders. Among the lymphoproliferative disorders related to infection by herpes virus 6 are: atypical polyclonal lymphoproliferation, non-Hodgkin lymphoma, hemophagocytic syndrome, among others. Finally, some researchers report the discovery of high antibody titers against herpes 6 in patients with myelodysplasia and chronic myeloproliferative syndromes (osteomielofibrosis and chronic myelogenous leukemia). Diagnosis The HHV6 can be isolated from patients with sudden rash during the febrile phase of the disease.

Samples are employed more often peripheral blood monocytes and saliva. These are inoculated on mononuclear cells prestimulated cord phytohemagglutinin. Furthermore, they can be used cell lines as HBS 2, the Sup T1 and Jurtka for variant A virus, and Molt 3 for variant B. The cytopathic effect appears between 5 and 9 days after inoculation the virus and is in rounding of the cells increase in size, merging with multinucleated giant cell formation and vacuolation. The virus can be confirmed by electron microscopy, immunofluorescence and immunoenzymatic assays for detecting antigens and molecular biology methods such as PCR and hybridization enable the detection of viral DNA in samples and in culture. Serological diagnosis is made by ELISA and indirect immunofluorescence using cells infected by the virus lymphoid origin. Epidemiology The herpesvirus 6 virus is ubiquitous in the human population. Is a lymphotropic virus that infects susceptible individuals during the first two years of life and generally cause lifelong latency. In a percentage variable, primary infection is followed by an acute illness of short duration, the sudden rash (children roseola or “sixth disease. ” The older individuals may suffer an illness similar to infectious mononucleosis or Kikuchi disease -Fujimoto. it is also capable of causing a wide range of hematopoietic, lymphoid and autoimmune disorders which have been associated with high titers of antibodies to the herpes virus 6 and of which the virus has been isolated. Maternal antibodies are generally present at birth and decline in the first months of life.

Seroconversion occurs in most cases between 6 and 18 months and the titles are high in adolescents. high titers of antibodies to herpes 6 have been observed in a number of diseases including immunocompromised persons; This suggests that reactivation of latent infection and exogenous reinfection occur with herpesvirus 6. So far it is assumed that herpesvirus 6 infection is transmitted by horizontal transmission through oropharyngeal secretions and there is no evidence of vertical transmission. Treatment Most primary infections do not require specific treatment. In case of related transplant recipients, fulminant hepatitis, hematopoietic disorders, autoimmune diseases lymphoid either the use of some antiviral. The virus is sensitive to foscarnet, ganciclovir and acyclovir relatively resistant.