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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human immunodeficiency virus infection of a human bone derived cell line was initiated by either cell free virus or with a cell to cell transmission method. The human bone derived cells were examined for 8 weeks, and virus infection was not detected when assessed by microscopy, immunofluorescence, reverse transcriptase activity, or infection of cocultivated human T lymphoid cells susceptible to human immunodeficiency virus. Polymerase chain reaction analysis of human bone derived cells inoculated with the cell to cell infection format showed less than 0.1% infected cells. It is possible that the infected cells detected by polymerase chain reaction were lymphocytes used in the cell to cell infection format. Alternatively, latent infection may have been established in the bone derived cells with no apparent expression of the proviral genome. A large proportion of bone is represented by human bone derived cells, and it is unlikely that bone will contribute to a significant human immunodeficiency virus reservoir in vivo. The blood of bone allograft donors is likely to have a greater virus bioburden than is bone. Methods to sterilize bone should be assessed by their efficacy to inactivate the virus in blood contaminating the graft, and methods to detect human immunodeficiency virus deoxyribonucleic acid in a bone graft may be less sensitive than examining the donor's blood.
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PMID:Human immunodeficiency virus infection of human bone derived cells. 889 52

Classification, structure and characteristics of neurotropic viruses are briefly summarized. Neurotropic viruses causing acute infection include Japanese, Venezuelan equine, and California encephalitis viruses, polio, coxsackie, echo, mumps, measles, influenza, and rabies viruses as well as members of the family Herpesviridae such as herpes simplex, varicella-zoster, cytomegalo and Epstein-Barr viruses. Those causing latent infection include herpes simplex and varicella-zoster viruses. Those causing slow virus infection include measles, rubella and JC viruses, and retroviruses such as human T-lymphotropic virus 1 and human immunodeficiency virus. Prion, which is not a virus but a host-derived non-physiological protein, causes transmissible spongiform encephalopathy such as kuru and Creutzfeldt-Jakob disease that resemble slow virus infection.
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PMID:[Neurotropic viruses--classification, structure and characteristics]. 910 70

Histoplasmosis is a common opportunistic infection in patients with human immunodeficiency virus (HIV) infection who reside in areas where Histoplasma capsulatum is endemic. We undertook a prospective study of a cohort of 304 HIV-Infected patients in Kansas City from October 1990 through March 1993 to define the incidence-specific risk factors, and pathophysiology of histoplasmosis. The annual incidence of histoplasmosis was 4.7%; 74% of the patients with histoplasmosis were symptomatic (all of whom had disseminated disease). A history of exposure to chicken coops, a positive baseline serology for complement-fixing antibodies to Histoplasma mycelium antigen, and a baseline CD4+ lymphocyte count of < 150/microL were associated with an increased risk for histoplasmosis. Histoplasmin reactivity and the presence of pulmonary calcifications were not useful markers for patients at high risk. Symptomatic infection occurred in 9.9% of patients with evidence of prior exposure to H. capsulatum, in 4.0% of patients without documented prior exposure, and in 3.0% of patients who were anergic; these findings suggest that the pathophysiology of histoplasmosis in patients with AIDS involves reactivation of latent infection in some cases and dissemination of exogenously acquired infection in other cases.
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PMID:Prospective study of histoplasmosis in patients infected with human immunodeficiency virus: incidence, risk factors, and pathophysiology. 919 82

This study was conducted with peripheral blood mononuclear cells from 67 human immunodeficiency virus (HIV)-infected adults. It supports the hypothesis that cross-linking of CD4 molecules by HIV gp120 can result in HIV upregulation and spread of infection. Underlying mechanisms include activation of latent infection by factors in addition to, or other than, tumor necrosis factor alpha.
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PMID:Upregulation of human immunodeficiency virus (HIV) replication by CD4 cross-linking in peripheral blood mononuclear cells of HIV-infected adults. 922 23

An animal model was used to assess whether resistance to superinfection by human immunodeficiency virus (HIV) can exist in vivo. Asymptomatic baboons (Papio cynocephalus), previously infected with HIV-2, were first challenged with homologous virus (HIV-2UC2 or HIV-2UC14) and later with heterologous virus (HIV-2UC12). After both virus inoculations, either resistance to viral infection or a transient viremia was observed. The original virus was recovered in 3 baboons, suggesting that reactivation of a latent infection occurred on heterologous challenge and that HIV-2 superinfection is blocked by processes established during prior infection. Antibody titers measured by ELISA and virus neutralization remained at low levels. However, suppression of HIV-1 replication was observed with CD8 T cells and filtered cell culture supernatants. The soluble factor involved was not a beta-chemokine. This resistance to HIV superinfection appears to be mediated at least in part by CD8 T cells that suppress virus production.
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PMID:Superinfection with human immunodeficiency virus type 2 can reactivate virus production in baboons but is contained by a CD8 T cell antiviral response. 933 53

As a result of a systematic review of non-Hodgkin's lymphoma of the gastrointestinal tract (GI) at the Yonsei University, Seoul, Korea and the Osaka University, Osaka, Japan, we found an extramedullary plasmacytoma in 5 of a total of 78 cases (6.4%) in Korea and 1 of 136 cases (0.7%) in Osaka, which represents an approximately 9-fold difference in frequency. The presence of the Epstein-Barr virus (EBV) genome was examined in paraffin-embedded specimens from the 5 cases with GI plasmacytoma from Korea together with 17 patients collected by a nationwide study in Japan. There were no clinical findings suggestive of the presence of immunodeficiency in these Korean and Japanese patients. There were no prominent differences in the age distribution or sex ratio between the patients of the two countries. Histologically, the proliferation of mature plasma cells was almost monomorphous with occasional bi- or multinucleated forms. The immunohistochemistry revealed a restricted cytoplasmic expression of immunoglobulin light chain, kappa type in 8 cases and lambda type in 14. A polymerase chain reaction of preserved DNA from 4 Korean and 16 Japanese patients found that only 2, both Korean, were positive for EBV of subtype A. The difference in the frequency of EBV positivity between Korean and Japanese cases was significant (p < 0.05). In situ hybridization revealed positive signals in the nucleus of the tumor cells. IHC revealed that the tumor cells in these two cases were positive for latent membrane protein-1 and EB nuclear antigen-2, showing latent infection of EBV. These findings suggest a close association of EBV and Korean GI plasmacytoma, and might partly explain the remarkable number of cases in this country.
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PMID:Plasmacytoma of the gastrointestinal tract in Korea: higher incidence than in Japan and Epstein-Barr virus association. 942 72

We have characterized the mechanism for human immunodeficiency virus type 1 (HIV-1) latent infection in a human T cell line MOLT-4 subclone no. 8 (MOLT-#8). The inocula used were HIV-1 recovered from MT-4 during the acute (NL-A) and persistent (NL-P) phases after HIV-1 infection. On infection of MOLT-#8 with NL-A, viral antigens first appeared in almost 100% of the cells whereafter the numbers of viable antigen-positive cells declined. In contrast, following infection with NL-P the expression of viral antigens was maintained in almost 100% of the cells. In fact, limiting dilution of NL-P-infected cells allowed us to isolate 43 subclones, all of which were positive for viral antigen expression in almost 100% of the cells (type I). In sharp contrast, only two of 41 subclones from NL-A-infected cells were of type I. Seven subclones were latently infected with HIV-1; latent HIV-1 in six subclones (type II), but not in one type III subclone, was activated by tumour necrosis factor (TNF)-alpha or phorbol 12-myristate 13-acetate. The remaining subclones were negative for the viral genome. Of particular note is the effect of endogenous TNF-alpha generated during the acute phase of virus replication which shifted the virus phenotype. Thus, the presence of TNF-alpha during the acute phase of virus replication seems to play a key role in the selective destruction of cells expressing higher levels of viral antigens and in subsequent establishment of latent infection in host T cells.
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PMID:Generation of endogenous tumour necrosis factor-alpha in MOLT-4 cells during the acute replication phase of human immunodeficiency virus type 1 determines the subsequent latent infection. 947 6

Common variable immunodeficiency represents the most frequently occurring primary immunodeficiency disorder and is usually detected sporadically in patients with no family history of immunodeficiency. We present the case stories of two monozygote twins, who following a period of decreasing serum immunoglobulins developed primary central nervous system lymphomas. One twin had clinical and paraclinical features mimicking multiple sclerosis. Immunohistochemical investigations on biopsy tissue showed expression of the bcl-2 and p53 gene products, and Epstein-Barr virus (EBV) encoded small RNA's (EBER) indicating latent infection were detected in lymphoma cells using in situ hybridisation techniques. The pathogenetic role of EBV in oncogenesis is discussed.
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PMID:EBV-positive primary central nervous system lymphomas in monozygote twins with common variable immunodeficiency and suspected multiple sclerosis. 949 19

These guidelines update previous CDC recommendations for the diagnosis, treatment, and prevention of tuberculosis (TB) among adults and children coinfected with human immunodeficiency virus (HIV) in the United States. The most notable changes in these guidelines reflect both the findings of clinical trials that evaluated new drug regimens for treating and preventing TB among HIV-infected persons and recent advances in the use of antiretroviral therapy. In September 1997, when CDC convened a meeting of expert consultants to discuss current information about HIV-related TB, special emphasis was given to issues related to coadministration of TB therapy and antiretroviral therapy and how to translate this information into management guidelines. Thus, these guidelines are based on the following scientific principles: * Early diagnosis and effective treatment of TB among HIV-infected patients are critical for curing TB, minimizing the negative effects of TB on the course of HIV, and interrupting the transmission of Mycobacterium tuberculosis to other persons in the community. * All HIV-infected persons at risk for infection with M. tubercu losis must be carefully evaluated and, if indicated, administered therapy to prevent the progression of latent infection to active TB disease and avoid the complications associated with HIV-related TB. * All HIV-infected patients undergoing treatment for TB should be evaluated for antiretroviral therapy, because most patients with HIV-related TB are candidates for concurrent administration of antituberculosis and antiretroviral drug therapies. However, the use of rifampin with protease inhibitors or nonnucleoside reverse transcriptase inhibitors is contraindicated. Ideally, the management of TB among HIV-infected patients taking antiretroviral drugs requires a) directly observed therapy, b) availability of experienced and coordinated TB/HIV care givers, and in most situations, c) use of a TB treatment regimen that includes rifabutin instead of rifampin. Because alternatives to the use of rifampin for antituberculosis treatment are now available, the previously recommended practice of stopping protease inhibitor therapy to allow the use of rifampin for TB treatment is no longer recommended for patients with HIV-related TB. The use of rifabutin-containing antituberculosis regimens should always include an assessment of the patient's response to treatment to decide the appropriate duration of therapy (i.e., 6 months or 9 months). Physicians and patients also should be aware that paradoxical reactions might occur during the course of TB treatment when antiretroviral therapy restores immune function. Adding to CDC's current recommendations for administering isoniazid preventive therapy to HIV-infected persons with positive tuberculin skin tests and to HIV-infected persons who were exposed to patients with infectious TB, this report also describes in detail the use of new shortcourse (i.e., 2 months) multidrug regimens (e.g., a rifamycin, such as rifampin or rifabutin, combined with pyrazinamide) to prevent TB in persons with HIV infection. A continuing education component for U.S. physicians and nurses is included.
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PMID:Prevention and treatment of tuberculosis among patients infected with human immunodeficiency virus: principles of therapy and revised recommendations. Centers for Disease Control and Prevention. 980 43

The number of cases with tuberculosis and human immunodeficiency virus infection is increasing in Japan. Tuberculosis is more likely to cause disease at an earlier stage of immunodeficiency, because M. tuberculosis is more virulent than other HIV-associated pathogens. Reactivation of latent infection has been traditionally considered the most important mechanism in the pathogenesis of active tuberculosis. However, recent exogenous infection may be higher among HIV-infected persons. The most striking clinical feature of tuberculosis in patients with HIV infection is the extremely high frequency of extrapulmonary involvement, usually with concomitant pulmonary tuberculosis. Among severely immunosuppressed patients with HIV infection, chest roentgenogram findings are hilar adenopathy, pleural effusions, and a miliary pattern. Antituberculosis therapy is effective in most patients with HIV infection.
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PMID:[Aids]. 988 44


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