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Query: UMLS:C0019693 (HIV)
170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of 33 cynomolgus monkeys (Macaca fascicularis) experimentally infected with Simian Immunodeficiency virus (SIV), strain smm3, 13 animals developed malignant Non-Hodgkin lymphomas. These lymphomas presented with unusual primary manifestations like in the orbita, testes, and brain. The morphological features and immunophenotyping identified the tumors as high malignant B-cell lymphomas. In all tumors as well as in tumor-derived cell lines a cynomolgus B-lymphotropic herpes virus (CBLV) with structural homogeneity to the Epstein-Barr virus (EBV) could be demonstrated by Southern blotting with EBV-specific probes. The lymphoma cells also expressed CBLV-associated nuclear antigens involved in B-cell transformation crossreacting with EBNA-specific human sera and monoclonal antibodies. Ig-gene rearrangement studies revealed clonal populations, however, no translocations of the c-myc oncogene could be detected. The lymphomas developing with high frequency in SIV-induced immunodeficiency resemble a major subtype of human EBV-associated AIDS lymphomas. This animal model can therefore be used to further elucidate interactions of HIV and EBV in AIDS-related lymphomagenesis.
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PMID:[Opportunistic malignant lymphomas in SIV infected primates--a model for Epstein-Barr virus associated lymphomas in AIDS]. 128 56

The paper provides an epidemiological characterization of HIV infection spread in a Russia's large region with more than 10 million people. The epidemiological findings show that the significant onset of HIV infection occurred among the population in this region in mid 1988. Homosexuals and bisexuals are prevalent among the HIV-infected, sexual contact is the main mode of HIV transmission. In addition to delivery of HIV infection from foreign countries, there are cases of local transmission. The clinical evidence indicates that most HIV-infected people are asymptomatic. Herpes viruses, Mycobacteria tuberculosis, Toxoplasma and fungi are common among causative agents of AIDS-related infections.
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PMID:[Clinico-epidemiological analysis of the cases of HIV infection in the north-western region of Russia]. 128 9

The British Paediatric Surveillance Unit is a joint undertaking of the British Paediatric Association, the PHLS Communicable Disease Surveillance Centre and the Department of Epidemiology at the Institute of Child Health, London. It provides an active case reporting system which aims to facilitate the surveillance of rare childhood infections and other conditions. Cards with a menu of up to twelve reportable disorders are sent monthly to more than 1100 paediatricians throughout the United Kingdom and Ireland. The average response rate is 90%. Reported cases are followed up according to study protocols. Since its inception in 1986, the Unit has facilitated the study of a wide range of disorders, including HIV infection and AIDS, Reye's syndrome, Kawasaki disease, congenital rubella, neonatal herpes, congenital toxoplasmosis and acute rheumatic fever, and the number of new applications for surveys has increased in 1992-3. Several European paediatric organisations have expressed interest in setting up similar schemes in their own countries.
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PMID:The British Paediatric Surveillance Unit: activities and developments in 1990 and 1991. 128 32

Many viruses cause opportunistic infections in HIV-positive patients. Those that cause oral lesions include herpes simplex, varicella zoster, Epstein-Barr virus, cytomegalovirus, and papillomavirus. Importantly, many of the herpes-group viruses are able to augment immunosuppression and some actually transactivate HIV replication-inducing genetic sequences. This article reviews the role of viral agents in the activation of HIV replication and details the features of the reported oral lesions that represent viral opportunistic infections.
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PMID:Viral infections of the head and neck among HIV-seropositive patients. 131 90

While it is now universally accepted that Ramsay Hunt syndrome is caused by varicella-zoster virus, Bell's palsy continues to be labeled "idiopathic." We review the literature associating Bell's palsy with various infectious agents as well as with Kawasaki disease, a condition in which an infectious etiology is suspected. Good evidence--mostly serological--exists for an etiologic role for the herpes group of viruses, mumps virus, and rubella virus. In addition, recent evidence has focused on Bell's palsy in human immunodeficiency virus infection and Lyme borreliosis. In view of the multiplicity of implicated agents, it is likely that the immunologic response associated with infection triggers a cranial or generalized polyneuropathy culminating in facial nerve compression, degeneration, and paralysis. The mounting interest in Bell's palsy, coupled with the increasing availability of more sensitive and specific tests, is likely to augment the available evidence for an infectious etiology and to clarify the role of other, previously unsuspected infectious agents.
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PMID:Facial palsy and infection: the unfolding story. 844 6

Verrucous skin lesions have been attributed to various herpes viruses in immunosuppressed patients, including those with human immunodeficiency virus infection (HIV). We examined such lesions from six HIV-infected patients to determine the range of microscopic findings present and to establish which herpesviruses were present. Verrucous epidermal hyperplasia, pseudocarcinomatous hyperplasia, and massive hyperkeratosis correlate with the warty clinical appearance of the lesions. Herpetic cytopathic changes, including multinucleated epidermal giant cells, steel-gray nuclei, necrotic acantholytic keratinocytes, and Cowdry type A nuclear inclusions were seen most prominently in the dells between papillations and in adnexal epithelium. In two cases, increased numbers of spindled cells were seen in the dermis. Immunoperoxidase staining with anti-type IV collagen antibodies demonstrated that these findings were not those of Kaposi's sarcoma, but represent a fibrotic reaction to the infection. Viral cultures of four of the cases demonstrated the presence of varicella-zoster virus, whose presence was detected by the polymerase chain reaction in paraffin-embedded lesional tissue from all six cases. Polymerase chain reaction did not show the presence of cytomegalovirus, herpes simplex, Epstein-Barr, or human papillomavirus. We conclude that these unusual verrucous lesions are a chronic manifestation of herpes zoster infection and that the reported presence of other agents in such lesions is probably coincidental.
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PMID:Chronic verrucous varicella-zoster virus infection in patients with the acquired immunodeficiency syndrome (AIDS). Histologic and molecular biologic findings. 132 20

In the current study, 35 pairs of corneas from asymptomatic carriers of HIV-1 and ten pairs from AIDS patients were analyzed for the presence of HIV-1 and HHV-6. The tissues were evaluated for viral antigens, transcripts, DNA sequences and intact and infectious virus. Three corneas from two asymptomatic carriers of HIV-1 and three corneas from two AIDS patients were culture positive for HIV-1. One of the three HIV-1 positive corneas from an asymptomatic HIV-1 carrier also was culture positive for HHV-6. Two of the tissue culture positive corneas from asymptomatic HIV-1 carriers and two from AIDS patients also tested positive for HIV-1 transcriptional activity by in situ hybridization. The label denoting the transcriptional activity was limited to stromal keratocytes. Most significantly, we were able to demonstrate the presence of HIV-1 particle(s) in sections and cultured PBMC from one of the HIV-1 culture positive corneas. PBMC from the same cornea also contained herpes virus particles. This report strengthens our earlier findings that HIV-1 and HHV-6 can invade corneal tissue, which emphasizes the importance of vigorous screening of corneal donors, specifically donors with HIV-1 exposure.
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PMID:Frequency of dual infections of corneas with HIV-1 and HHV-6. 132 27

This review discusses current reports on herpes simplex virus infections as they relate to the use of laboratory testing, infections in the neonate, herpes simplex virus association with human immunodeficiency virus infection, and updating the current therapy and management of genital herpes. Findings over the past year are important in the clinical management of patients with genital herpes. All health care workers who manage patients with genital herpes need to know the limitations of serologic testing. Current information suggests that serologic commercial testing that is most commonly available cannot discriminate between infections caused by herpes simplex virus type 1 and type 2. Laboratory methods still rely on culturing herpes simplex virus in living cells in vitro. However, the availability of monoclonal antibodies allows for rapid assays for the confirmation of cultured herpes simplex virus. In addition, assays have been developed and tested, suggesting that perhaps antigen-detection systems may be available that could replace culturing the virus in living cells. New information on neonatal herpes points out the predictors of morbidity and mortality in newborns who contract herpes within the first few weeks of life. Information concerning asymptomatic shedding in labor will provide the clinician with a better understanding of this disease entity in the pregnant woman. Several studies have confirmed that herpes simplex virus infection is a risk factor for developing human immunodeficiency virus infection. A new study clearly shows that treatment using daily acyclovir therapy over a prolonged period of time can control and may modify herpesvirus infection.
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PMID:Herpes simplex virus infections. 132 52

Four patients with acquired immunodeficiency syndrome, a 27-year-old female intravenous drug abuser and three males (two drug addicts aged 27 and 33 years and a 40-year-old homosexual) presented with a rapidly progressive encephalopathy. Two had generalized varicella-zoster virus skin infection, one had had a regressive thoracic zoster rash 7 months previously and one had no history of cutaneous eruption. Neuropathological examination revealed, in each case, multifocal necrotic changes with numerous, intranuclear Cowdry type A inclusion bodies in glial cells, endothelial cells, macrophages and neurons, within and around the lesions. These inclusion bodies were stained positively for varicella-zoster virus by immunocytochemistry and contained herpes virus nucleocapsids by electron microscopy. Molecular biology using the polymerase-chain-reaction method demonstrated viral genome. In one case, zoster-induced non-inflammatory vasculopathy involved medium sized leptomeningeal vessels and was associated with circumscribed areas of cortico-subcortical infarction. In another case, varicella-zoster virus encephalitis was associated with human immunodeficiency virus encephalitis and a secondary cerebral lymphoma. Multinucleated giant cells expressing human immunodeficiency virus proteins in their cytoplasm, were found in the lymphomatous deposits and in the varicella-zoster virus necrotic lesions. In these latter lesions, Cowdry type A inclusion bodies could be seen in the nuclei of some multinucleated giant cells confirming previous observations of MGCs co-infected by HIV and CMV, and supporting the hypothesis that DNA viruses interact with HIV, thus increasing its effect.
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PMID:Varicella-zoster virus encephalitis in acquired immunodeficiency syndrome: report of four cases. 133 72

After a review of the literature reports from recent years viral infections in pregnant women are presented as a fetal and neonatal risk factor. Maternal infections with rubella virus, cytomegalovirus++, hepatitis, Coxsackie B, varicella, herpes, poliomyelitis, parvovirus B19 and HIV are discussed stressing their unfavourable effect on the developing embryo, fetus or newborn.
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PMID:[Maternal viral infections as a fetal risk factor]. 133 11


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