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

Chronically immunosuppressed individuals are susceptible to lymphoreticular tumors. Up to 15% of patients with congenital deficiencies such as ataxia=telangiectasia may develop malignancies, mainly high-grade B cell non=Hodgkin's lymphomas (NHLs). AIDS lymphomas are comprised of NHLs including Burkitt's lymphoma (BL) and primary cerebral lymphomas (PCLs). Almost 3% of all AIDS patients (2824 of 97,258 cases) developed NHL. Epstein-Barr virus (EBV) as a co-factor in AIDS lymphomagenesis has been studied: in 12 cases of 24 AIDS lymphomas EBV by DNA in situ hybridization was found. In an analysis of 6 primary cerebral lymphomas, .5 were positive for EBV DNA by Southern blotting. In Burkitt's lymphoma the characteristic genetic alteration affects the c-myc oncogene. In 1/3 of BL p53 mutations were found but none in the 43 NHLs suggesting that p53 mutations and c-myc activation act synergistically in the pathogenesis of these tumors. Cytotoxic agents dideoxyinosine, dideoxycytosine, and zidovudine may cause secondary neoplasia. 8 of 55 AIDS patients under zidovudine treatment developed high-grade lymphoma 23.8 months subsequently; recently doses were reduced. PCL was found in 21 of 90 patients. A 5.2 months survival was associated with combined treatment with cyclophosphamide, Oncovin (vincristine), methotrexate, etoposide, and cytosine arabinoside compared with 11.3 months with chemotherapy. Colony-stimulating factors (CSFs) alleviate drug-induced myelotoxicity and zidovudine-induced neutropenia, however, l8 of 11 patients receiving granulocyte-macrophage CSF developed hematological toxicity. Interleukine-2 produced by T-helper cells enhancing tumor cells cytotoxicity has been used in AIDS-associated cryptosporidial diarrhea and in 4 patients with AIDS lymphoma with modest response, but its stimulation of the HIV-infected substrate may increase viral proliferation.
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PMID:AIDS lymphomas. 161 63

Nonherpetic encephalitis outside the newborn period is usually a self-limited disease. The majority of patients will recover without significant sequelae, and require only supportive therapy during the acute illness. Though the underlying viral etiology frequently will escape detection, identification of the infecting agent has considerable prognostic value which can complement clinical measures of severity of disease. The most important initial task of the clinician faced with a case of presumptive viral encephalitis is to eliminate the possibility of a treatable illness. Once this has been done, the diagnosis of viral encephalitis can be supported by documenting the characteristic slow-wave background activity on EEG, and a mild lymphocellular pleocytosis in the CSF. Because viral encephalitis can be caused by such a large number of organisms, the search for an etiology can be daunting. Realizing that all the agents described above can, at times, cause encephalitis without any clue to their identity, one nevertheless may use several pieces of historical information to narrow the possibilities. Travel history, animal exposures, immunization history, and seasonality all may help to steer the search in a particular direction and, indeed, may point to a nonvirologic cause as well. In addition, detection of extraneurological signs and symptoms may strongly indicate a specific virologic diagnosis. Finally, knowledge of concurrent community epidemic patterns, and of surveillance data routinely collected by local and state health departments, can help to increase or decrease the likelihood of a given pathogen. The causative viral agent usually can be identified by serological testing and viral culture. Occasionally, single serological determinations are diagnostic: in rabies (when the patient has not received immune prophylaxis), eastern equine encephalitis, and HIV, since seropositivity is strongly associated with symptomatic illness; and in Epstein-Barr virus, if a panel of antibody determinations which can time the infection is available. In addition, high CSF: serum titers for antibody against any neurotropic agent is usually diagnostic, though the absence of a high central nervous system antibody titer does not eliminate any potential viral pathogen. With these few exceptions, a single serological determination for a given pathogen is almost always impossible to interpret; paired sera (one obtained upon diagnosis, and one obtained 10 to 14 days later, either just prior to hospital discharge or at a follow-up visit) are far more helpful. Many viruses that directly infect the central nervous system are difficult to recover from the CSF; therefore, viral isolation from the nasopharynx and stool also should be sought.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Viral encephalitis. 164 66

Hairy leukoplakia (HL) also occurs in immunosuppressed post-bone-marrow transplantation patients, and in the presence or absence of Epstein-Barr virus. It may not always be diagnostic of HIV positivity. However, HIV status should still be determined in patients with HL.
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PMID:Hairy leukoplakia-like lesions following bone-marrow transplantation. 164 86

The fact that viruses can cause cancer in animals has been appreciated since the turn of the century. The widely held belief that viruses had little to do with cancer in humans has only recently been dispelled. Two classes of human retrovirus (HTLV and HIV) have been discovered in the last decade and the malignant potential of hepatitis B virus, Epstein Barr Virus and the human papilloma virus have been documented not only by confirming their association with disease by large scale epidemological studies but also at the molecular level. Indeed detailed investigation of the way viruses can cause cancer can reveal new insights into 'final common pathways' and hopefully provide new approaches for treatment over and above the real possibility that virus associated cancers can potentially be vaccinated against.
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PMID:Viruses and cancer. 165 Jun 23

Viral cofactors may be important in the pathogenesis of HIV infection and the development of AIDS, but their role is still imperfectly understood. Sequential serological studies were performed in a cohort of 100 homosexual men and 70 matched healthy controls over a mean period of 4 years. Of the patients, 18 were found to be HIV+ on admission to the study and 15 seroconverted to HIV+ during the follow up (seroconversion group). Serum antibodies of both IgG and IgA isotypes against Epstein-Barr virus (EBV) and cytomegalovirus (CMV) were determined. IgG antibodies indicate past infection, while a marked increase in IgG titre or a positive IgA titre were taken to indicate active infection or reactivated latent infection. EBV and CMV infections were about two to four times more prevalent in the homosexual men both HIV- and HIV+, compared with controls. Active infections were increased in the homosexual men and particularly in the HIV+ patients. The seroconversion group revealed activation of both EBV and CMV following HIV infection. When the antibody profile of seroconverting patients at the time preceding seroconversion was compared with a matched group of 39 homosexual men who remained HIV-, no change was found in CMV antibodies, but four out of 15 (26.6%) of the patients had high titres of anti-EBV IgA preceding seroconversion, as compared with only one out of 39 (2.6%) of HIV- homosexual men (P less than 0.05). This suggests a role for EBV reactivation in the pathogenesis of HIV infection in some patients.
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PMID:Sequential serological studies of homosexual men with and without HIV infection. Epstein-Barr virus activation preceding and following HIV seroconversion. 165 Jun 55

Reactivation of Epstein-Barr virus (EBV) in early human immunodeficiency virus (HIV) infection was investigated in 49 homosexual men who seroconverted to HIV (cases) as compared with 49 matched controls who remained seronegative to HIV during a longitudinal study. EBV infection was reactivated in cases 6 months, but not 12 months, prior to HIV seroconversion as compared with controls and remained reactivated during 18 months of follow-up after HIV seroconversion, as shown by increases in immunoglobulin (Ig) G antibody titers to EBV early antigen. Antibody titers to EBV viral capsid antigen did not differ between cases and controls prior to the time of seroconversion to HIV but were significantly increased among cases by the first seropositive study visit and remained elevated during the 18 months after HIV seroconversion. Total serum IgG levels were increased in cases at the visit of seroconversion, and during 18 months of follow-up, but did not correlate with enhanced IgG production specific for EBV antigens. Significant decreases in numbers of CD4+ cells and increases in numbers of CD8+ cells during this early phase of HIV infection were not associated with changes in patterns of EBV antibody responses. Reactivation of EBV beginning 6 months before HIV seroconversion may have implications regarding the role of this herpesvirus in the pathogenesis of HIV.
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PMID:Reactivation of Epstein-Barr virus during early infection with human immunodeficiency virus. 165 Jul 90

The pathogenesis of the HIV-associated lymphomas is not well understood. In order to begin characterizing this class of lymphoma, we initiated a molecular genetic study of DNA extracted from 31 diagnostic biopsy specimens from patients diagnosed with AIDS-associated non-Hodgkin's lymphoma. Analysis of 25 peripheral lymphomas showed that 14 were monoclonal B-cell processes, while 11 appeared to be of polyclonal origin. Five of the 14 monoclonal lymphomas were found to have rearrangements of the c-myc gene. Epstein-Barr virus (EBV) genomes were found in seven out of 14 monoclonal samples, but only two out of nine polyclonal samples. The six primary central nervous system (CNS) lymphoma samples were more homogeneous than the peripheral samples and all were monoclonal, positive for EBV and lacked detectable c-myc gene rearrangements. This study allows us to subdivide the HIV-associated lymphomas into three major molecular subtypes: (1) monoclonal B-cell process frequently associated with c-myc rearrangement or detectable EBV genomes, (2) polyclonal B-cell process typically without evidence of EBV, and (3) monoclonal primary CNS process associated with EBV genomes and lacking detectable c-myc rearrangement.
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PMID:Evidence for molecular subtypes of HIV-associated lymphoma: division into peripheral monoclonal, polyclonal and central nervous system lymphoma. 165 78

Double infection of cells by HHV-6, Epstein-Barr virus (EBV) and by human immunodeficiency virus (HIV-1) can enhance viral effects though genetic transactivation. It remained to be clarified, however, by which mechanism different viruses may enter the same cell. We have shown that HHV-6 infection of immature lymphoid cells rigidifies the cytoplasmic membrane and causes receptor proteins for viruses such as CD4 for HIV-1 and CR2 for EBV to be expressed. In our experiments, HHV-6 infected cells were superinfected by HIV1 and caused enhanced cell death. The mechanisms by which receptors were expressed after HHV-6 infection appears independent of cell membrane rigidification alone and is suppressed by cycloheximide only to a certain extent.
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PMID:Human herpesvirus-6 infection may predispose cells to superinfection by other viruses. 165 48

Burkitt's lymphoma (BL) is a highly malignant B cell tumor characterized by three types of chromosomal translocation which constitutively activate the c-myc oncogene by juxtaposing it to Ig coding sequences. Epstein-Barr virus (EBV) infection, hyperendemic malaria and HIV-caused immunosuppression are thought to contribute to the pathogenesis of the tumor. Cell lines derived from EBV carrying and EBV negative BLs often show altered MHC class I antigen expression. The defects include a lower expression of all HLA class I antigens compared to EBV transformed normal B-blasts, and selective down-regulation of certain HLA-A and HLA-C alleles. As a consequence BL cells are often resistant to cytotoxic T lymphocyte (CTL) mediated destruction. Alleles selective down-regulations are found only in cell lines that maintain the tumor cell phenotype while shift towards a more activated 'B-blast like' phenotype is accompanied by HLA class I up-regulation. A similar pattern of HLA class I expression can be found in a subpopulation of germinal center B cells which express a 'BL like' phenotype. Our findings suggest that the HLA class I expression of BL cells reflects the characteristics of the normal B cell precursor and is probably not the result of immune selection.
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PMID:Cell phenotype dependent expression of MHC class I antigens in Burkitt's lymphoma cell lines. 165 15

Hairy leukoplakia is a recently described oral mucosal condition seen in immunosuppressed individuals, usually in association with HIV infection, when it is thought to be a sign of decreasing immunocompetence. It probably results from reactivation of infection by Epstein-Barr virus (EBV) and usually presents as bilateral white patches on the lateral borders of the tongue. From a histological study of 20 cases we have found that the typical appearance of hairy leukoplakia is of acanthotic, hyperparakeratinized epithelium with Candida hyphae sometimes present in the parakeratin. A band of EBV infected, koilocyte-like cells is present in the upper part of the prickle cell layers, these cells being swollen and pale staining, with prominent cell borders and perinuclear vacuoles. There is a paucity of inflammation in both the epithelium and lamina propria. An atypical appearance shows the koilocyte-like cells lying isolated or in small groups, irregularly arranged in the prickle cell layer and without a hyperparakeratinized surface. Diagnosis of hairy leukoplakia should normally be confirmed by demonstrating EBV in the koilocyte-like cells by immunocytochemistry or DNA in situ hybridization.
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PMID:Hairy leukoplakia--a histological study. 157 18


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