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

A study was conducted to assess the occurrence of latent infection with the human immunodeficiency virus (HIV) among seronegative people at high risk of infection. The presence of HIV genomes was analysed by molecular techniques in two seronegative children born to mothers infected with HIV and in three regular sexual partners of seropositive drug addicts. The adults were selected from a seronegative cohort at high risk of infection because of their sexual contacts and the children selected because of impaired growth. HIV retroviral sequences were detected in four of the five subjects directly at the cellular level by in situ hybridisation in peripheral blood mononuclear cells. HIV genomic sequences were confirmed by in vitro amplification of viral DNA with the polymerase chain reaction technique. The existence of a latent viral infection state in these seronegative subjects indicates the unreliability of standard serological analysis in people who have been in regular contact with infected patients.
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PMID:HIV viral sequences in seronegative people at risk detected by in situ hybridisation and polymerase chain reaction. 249 18

Human herpesvirus-6 (HHV-6), formerly known as human B-lymphotropic virus (HBLV), was first isolated in 1986 from patients with lymphoproliferative disorders and AIDS. Antibody prevalence against HHV-6 varies between about 60-80% indicating a widespread latent infection. Although HHV-6 infects in vivo primarily T-lymphocytes, it is associated with similar diseases as in infection with Epstein-Barr virus (EBV), a clearly B-lymphotropic virus. Reactivation of latent HHV-6 infection in patients with subnormal host defense may cause persistent active infection with so-called postinfectious chronic fatigue syndrome (PICFS) or may contribute to other pathologies such as immune deficiency itself, autoimmune disorders or progressive lymphoproliferation. Coinfection of CD4 cells by HHV-6 and human immunodeficiency virus (HIV 1) in AIDS patients can aggravate HIV-induced acquired immune deficiency. These characteristics of the only recently detected new virus justify further intense investigation.
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PMID:What's new in human herpesvirus-6? Clinical immunopathology of the HHV-6 infection. 255 96

Evidence of a latent human immunodeficiency virus type 1 (HIV-1) infection in healthy, seropositive individuals who do not have viral antigens in their sera and from whom virions cannot be rescued in cocultivation experiments was examined. Proviral DNA was detected by amplification by the polymerase chain reaction procedure. In each of 10 seropositive individuals, the presence of HIV-1 proviral sequences was demonstrated in their peripheral blood mononuclear cells. By using fluorescence-activated cell sorting, we obtained highly enriched subpopulations of peripheral blood mononuclear cells and found that the CD4+ T-cell subset is the cell subset that consistently harbors the HIV-1 proviral sequences. The number of HIV-1-infected CD4+ T cells was variable among the 10 healthy individuals, ranging from 1 in 100 to 1 in 40,000. While in vitro infection of CD4+ T cells causes down regulation and eventual loss of CD4 surface molecules, this is not true in vivo where it is only the CD4+ population that harbors the virus. This disparity may reflect differences between a latent infection in vivo with the lytic response of cells infected in vitro.
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PMID:Integrated proviral human immunodeficiency virus type 1 is present in CD4+ peripheral blood lymphocytes in healthy seropositive individuals. 279 14

We have developed a nucleic acid hybridization assay for detecting human immunodeficiency virus (HIV) RNA in peripheral blood mononuclear cells. This assay can detect HIV RNA in 10(2) cultured lymphoblastoid cells infected with HIV; it only weakly crossreacts with the RNA of HTLV-I or HTLV-II. For 39 (80%) of 49 seropositive subjects, we detected HIV sequences in the RNA from 10(6) peripheral blood mononuclear cells. In contrast, we could not detect HIV DNA in samples of DNA from the same number of cells from any of 39 seropositive individuals tested. Three of 33 seronegative individuals had false-positive results. Nevertheless, because we found an excellent correlation between results from our assay and culture of HIV from peripheral blood mononuclear cells of seropositive subjects, it is unlikely that positive cultures of HIV from these cells reflect latent infection. Nucleic acid hybridization offers a more rapid, simple, and inexpensive alternative to culture for detecting HIV-infected peripheral blood mononuclear cells.
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PMID:Detecting human immunodeficiency virus RNA in peripheral blood mononuclear cells by nucleic acid hybridization. 282 Nov 28

Cats exposed to the feline leukemia virus (FeLV) may mount an effective immune response and eliminate the virus, develop a non-viremic, latent infection or become persistently infected and shed the virus. Persistently infected cats commonly die of secondary opportunistic infections that result from FeLV-induced immunosuppression. The acquired immunosuppression is the most frequent and most devastating consequence of FeLV infection in the cat. Immunosuppression is targeted primarily to the cell-mediated immune system and has been attributed to the viral p15e envelope protein. The decreased IgG response and proliferative response to T cell mitogens is thought to be due to a defect in the helper cell function. As a result of T helper cell immunosuppression, infected cats may also have defective cytotoxic lymphocyte and activated macrophage functions which are regulated by their lymphokines. Research has shown that the virus causes a general suppression in the production of T cell-derived lymphokines, including gamma interferon and interleukin 2. A decrease in the function of polymorphonuclear leukocytes has also been reported and may contribute to deaths due to opportunistic infections in FeLV-positive cats. There are numerous parallels between the acquired immunodeficiency syndrome (AIDS) in man and the FeLV-induced immunodeficiency syndrome in cats. Frequent deaths due to opportunistic infections, lymphopenia, depressed cell-mediated immune responses to T cell-dependent antigens despite hypergammaglobulinemia and the presence of a long period of time between infection and the onset of clinical signs are just a few of the syndromes that are similar between the 2 retroviral diseases. A new strain of FeLV, FeLV-FAIDS has been associated with a naturally occurring immunosuppressive syndrome that is strikingly similar to AIDS in man. In addition, a T-lymphotropic retrovirus has recently been identified from cats with an immunodeficiency-like syndrome; this feline lentivirus disease is morphologically similar, but antigenically distinct from the human immunodeficiency virus, the cause of AIDS. Treatment for FeLV immunosuppression is primarily supportive. The development of a soluble tumor cell antigen vaccine has been shown to be efficacious in preventing FeLV infections.
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PMID:Clinical and immunologic aspects of FeLV-induced immunosuppression. 284 93

Human immunodeficiency virus (HIV) establishes latent infection in CD4 lymphocytes and macrophages. It can destroy CD4 cells by direct virus cytotoxicity, indirectly through the host response against HIV-infected cells, or by both means. Cells of the macrophage lineage are generally not destroyed but can serve as a reservoir of virus. HIV also causes functional impairment in remaining infected and uninfected cells. After exposure to infection by sexual, blood or maternofetal contact, about half the contacts become infected with HIV. Factors influencing the inoculum derived from the infected person include type of contact, phase of infection and local factors enhancing HIV replication or excretion. In the exposed person, genetic factors and systemic or local events such as infection or inflammatory injury may influence relative susceptibility. After infection with HIV, a number of outcomes may be seen, including symptomless carriage, with or without lymphadenopathy, or symptomatic disease, including the AIDS-related complex, acquired immune deficiency syndrome and HIV encephalopathy. Infection, multiple pregnancy and infancy are associated with increased or more rapid progression to symptomatic disease; malnutrition and immunosuppressive drugs may exert a similar effect. Genetic factors appear to affect disease susceptibility. Mechanisms influencing progression can be divided into those affecting the rate of HIV replication, those that determine the host response to HIV, and those mediated by other immunosuppressive influences. The host's balance with HIV thus resembles that of a tightrope walker, any force tending to tip him towards a catastrophic and irretrievable decline.
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PMID:Factors affecting the natural history of human immunodeficiency virus infection. 290 7

The incidence of tuberculosis (TB) among inmates of the New York State prison system increased from 15.4 per 100,000 in 1976 through 1978 to 105.5 per 100,000 in 1986. Matching of TB and acquired immunodeficiency syndrome registries indicated that the majority (56%) of inmates with TB reported in 1985 and 1986 had acquired immunodeficiency syndrome or human immunodeficiency virus infection; none were known to be human immunodeficiency virus seronegative. A case-control study examined 59 inmates with TB reported from 1984 through 1986 and 59 matched control inmates without TB. Inmates who reported street drug use were more likely to develop TB: odds ratio, 9.7; 95% confidence interval, 2.8 to 33.6 and odds ratio, 7.3; 95% confidence interval, 0.9 to 59.3 by unconditional and conditional logistic regression analyses, respectively. Although the majority of cases are thought to be due to reactivation of latent infection, phage typing of 16 Mycobacterium tuberculosis cultures suggested the possibility of inmate-to-inmate transmission in at least one cluster of three cases. It is of crucial importance that TB control measures be reinforced in the prison setting to counter the increased risk created by human immunodeficiency virus infection.
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PMID:Increasing incidence of tuberculosis in a prison inmate population. Association with HIV infection. 274 10

Human immunodeficiency virus (HIV) is the causative agent of the acquired immune deficiency syndrome (AIDS). A large number of AIDS patients show evidence of neurologic involvement, known as AIDS-related subacute encephalopathy, which has been correlated with the presence of HIV in the brain. In this study, two genetically distinct but related viruses were isolated from one patient from two different sources in the central nervous system: brain tissue and cerebrospinal fluid. Both viruses were found to replicate in peripheral blood lymphocytes, but only virus from brain tissue will efficiently infect macrophage/monocytes. The viruses also differ in their ability to infect a brain glioma explant culture. This infection of the brain-derived cells in vitro is generally nonproductive, and appears to be some form of persistent or latent infection. These results indicate that genetic variation of HIV in vivo may result in altered cell tropisms and possibly implicate strains of HIV with glial cell tropism in the pathogenesis of some neurologic disorders of AIDS.
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PMID:Dual infection of the central nervous system by AIDS viruses with distinct cellular tropisms. 364 51

We report a new case of acquired immune-deficiency syndrome (AIDS) in a 43 year-old white homosexual man, characterized by the association of disseminated cutaneo-mucous Kaposi's sarcoma and cerebral toxoplasmosis. This man had Kaposi's sarcoma for about 10 years but evolution became quickly extensive in July 1981. Chlorambucil was prescribed at that time and was the cause of a pancytopenia. Death occurred in July 1982 due to a cerebral mass identified as toxoplasmosis on a left temporal biopsy. This observation is typical of AIDS, a new syndrome which suddenly developed in the last 2 years in the United States in homosexual men, Haitians and hemophiliacs, and is characterized by disseminated Kaposi's sarcoma and/or opportunistic infections, with a very high mortality rate. Severe toxoplasmosis of CNS has been reported in AIDS and appears to result from defects in cellular immunity which permit recrudescence of latent infection. Cerebral biopsy is necessary for the diagnosis of cerebral toxoplasmosis as seroconversion occurs infrequently in immuno-suppressed hosts. AIDS appeared in Western Europe in 1982. Most of the cases were reported in France, Denmark, Belgium and Great Britain. These cases differ from reported cases in the USA: fewer drug or poppers users, fewer homosexual men, an important number of people having lived or travelled in the Kaposi's endemic area (Mediterranean basin and Central Africa). The immunological profile of patients presenting AIDS in Europe doesn't seem to differ from the american profile: serious cellular immunodeficiency and marked increase in the suppressor/cytotoxic cell population. As in the United States, one may suspect, among several hypotheses, that it is caused by one or several transmissible agents now present in France. The nature of these agents, transmissible by sexual contacts and blood, is not yet known: the role of the CMV is now less probable and most of the studies look for the role of other factors such as the HTLV.
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PMID:[Acquired immunodeficiency syndrome, Kaposi's disease and cerebral toxoplasmosis in a young man. Review of the literature apropos of a case]. 637 20

Pneumocystis carinii hominis is a ubiquitous organism that causes pneumonia in immunocompromised persons. Paired P. carinii hominis isolates from human immunodeficiency virus-infected persons who had two episodes of pneumocystosis were examined for genetic heterogeneity. Genetic variation was detected by sequence comparison of a portion of the mitochondrial ribosomal RNA gene. In 5 of 10 patients experiencing two episodes of pneumocystosis, genetically distinct isolates were associated with each episode. These included 4 of 6 patients whose second episode of pneumocytosis occurred > 6 months after their initial bout. The genetic data support the hypothesis that some recurrent episodes of P. carinii hominis pneumonia are caused by reinfection rather than by reactivation of latent infection.
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PMID:Genetic variation among Pneumocystis carinii hominis isolates in recurrent pneumocystosis. 754 88


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