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Query: UMLS:C0021051 (
immunodeficiency
)
71,517
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
2',3'-Didehydro-2',3'-dideoxy-5-chlorocytidine (D4CC) is, in contrast with 2',3'-dideoxy-5-chlorocytidine (ddClCyd) and 2',3'-didehydro-2',3'-dideoxy-5-chlorouridine (D4CU), a potent and selective inhibitor of the replication of human
immunodeficiency
virus (HIV) types 1 and 2, simian
immunodeficiency
virus (SIV) and
simian AIDS
related virus (SRV). D4CC is a poor inhibitor of the phosphorylation of [5-3H]2'-deoxycytidine (dCyd) by partially purified MT-4 cell dCyd kinase (Ki: 612 microM). The findings that (i) D4CC has little, if any, affinity for MT-4 cell Cyd/dCyd deaminase, (ii) D4CU is not antivirally active and (iii) the antiretroviral action of D4CC can be reversed by dCyd, but not dThd, indicate that D4CC is antivirally active as its Cyd metabolite (D4CC 5'-triphosphate) and does not need to be deaminated (to the corresponding Urd metabolite) to exert its antiretroviral action.
...
PMID:2',3'-didehydro-2',3'-dideoxy-5-chlorocytidine is a selective anti-retrovirus agent. 259 Jan 97
The identification of human
immunodeficiency
virus (HIV)-2 has given rise to difficulties that were not anticipated when HIV-1 was thought to be the only virus involved in acquired immunodeficiency syndrome (AIDS). HIV-2, which seems to be prevalent only in Africa, differs from HIV-1 in its envelope and core proteins, and is more closely related to the
simian AIDS
virus than to HIV-1. Commercial assay kits that use HIV-2 antigen to detect anti-HIV-2 are available from only 1-2 manufacturers, although the cross-reactions between HIV-2 antibody and HIV-1 antigen probably allow most HIV-2 infections to be recognized by existing anti-HIV-1 assays. Until more HIV-2 infections are found in Europe and the US, unselected screening of blood donors for HIV-2 would be hard to justify. At present, testing of donors with West African connections and exclusion of those who have had sexual contacts in sub-Saharan Africa are probably sufficient measures to protect recipients in developed countries from HIV-2. More information is needed in 2 areas: HIV-2 infection in Africa and its effects, and the possible range of retrovirus infection in blood donors.
...
PMID:HIV-2 in perspective. 289 72
Fifty percent of primates with acquired
immunodeficiency
caused by a well-characterized type D retrovirus (
SAIDS
D) developed clinical, laboratory, and histologic features of polymyositis. By use of specific antisera and immunochemical techniques, we found the virus in the lymphoid cells surrounding muscle fibers and invading the endomysia septa.
SAIDS
D virus was isolated from the involved muscles and infected myotubes of normal muscle in tissue culture. These results suggest that retroviruses, a group of viruses increasingly associated with human diseases, can cause polymyositis with
immunodeficiency
in nonhuman primates and could play a role in human polymyositis.
...
PMID:Polymyositis in an immunodeficiency disease in monkeys induced by a type D retrovirus. 300 28
A spontaneous multifocal subcutaneous fibromatosis is described in 6 pig-tailed macaques (Macaca nemestrina) with simian acquired immune deficiency syndrome (
simian AIDS
). The lesions consisted of a proliferation of vascular fibrous tissue that was infiltrated by lymphocytes and plasma cells. One animal also had retroperitoneal fibromatosis, which has also been found in this colony of pig-tailed macaques. Progressive weight loss, diarrhea, lymphadenopathy, and neutropenia were seen. Peripheral lymph nodes were hyperplastic, and there was splenomegaly. Aggregates of lymphocytes were present in the bone marrow, kidneys, liver, and lungs. Type D retrovirus particles were found in three nodules by electron microscopy; intracytoplasmic type A and budding particles were identified in fibroblasts. In a setting of acquired
immunodeficiency
, these subcutaneous tumors in pig-tailed macaques present a striking analogy to Kaposi's sarcoma in human AIDS.
...
PMID:Subcutaneous fibromatosis associated with an acquired immune deficiency syndrome in pig-tailed macaques. 401 42
This paper reviews the major features of a simian model of acquired
immunodeficiency
('
SAIDS
'),
SAIDS
occurs endemically in colonies of macaque monkeys in the United States and resembles AIDS in humans in overall clinical manifestations, pathology, and immune deficiency. An infectious type D retrovirus, related to but distinct from the Mason-Pfizer monkey virus, has been identified as the primary cause of
SAIDS
. The relevance of these findings for human AIDS is discussed.
...
PMID:Simian AIDS--evidence for a retroviral etiology. 609 Feb 98
A novel type D retrovirus was isolated by cocultivation of explants of fibromatous tissue from a rhesus monkey (Macaca mulatta) with
immunodeficiency
and retroperitoneal fibromatosis. This type D virus, isolated from a macaque with simian acquired immunodeficiency syndrome (
SAIDS
-D/Washington), is exogenous and is partially related to the Mason-Pfizer and the langur monkey type D viruses. The SAiDS-D virus can be distinguished from all other primate retroviruses by antigenicity and molecular hybridization. Nucleic acid hybridization studies reveal that the origin of the
SAIDS
-D isolate may reside in Old World monkey (subfamily Colobinae) cellular DNA.
...
PMID:Characterization of exogenous type D retrovirus from a fibroma of a macaque with simian AIDS and fibromatosis. 620 Sep 29
While it has been demonstrated that the Nef protein of simian
immunodeficiency
virus is obligatory for the establishment of high viral loads and the development of
simian AIDS
in rhesus macaques, demonstrating a critical role for the human
immunodeficiency
virus (HIV) Nef protein in tissue culture has been elusive. Data have been contradictory as to whether Nef has a negative or positive influence on in vitro virus replication. In an attempt to define a role for Nef during virus propagation in tissue culture and to obtain virus-host systems that could distinguish between the Nef mutant and wild-type viruses, we have introduced mutations into the nef genes of infectious molecular clones of three HIV-1 strains and two isolates of the HIV-2ROD strain and have investigated the capacity of viruses derived from them to infect a number of CD4-positive T-cell lines and peripheral blood mononuclear cells (PBMC). Mutating the nef gene of all viruses had a modest negative effect on virus production in activated PBMC. In some T-cell lines with some viruses, the effects were severe, and little or no Nef mutant virus could be detected. In other cell lines, the result of mutating the nef gene either had no effect or had a slight negative effect on the replication kinetics. Therefore, whether the consequences of loss of Nef activity can be demonstrated in vitro depends on both the particular virus and the host cell used, suggesting that Nef is exerting its activity on some cellular pathway. In addition, we describe the construction and properties of hitherto unreported infectious molecular clones of the ROD strain of HIV-2.
...
PMID:Both virus and host components are important for the manifestation of a Nef- phenotype in HIV-1 and HIV-2. 748 59
To evaluate the role of humoral immunity against simian
immunodeficiency
virus (SIV), we tested whether passive immunization with plasma from SIVmac251 vaccine-protected or healthy infected animals would protect rhesus monkeys against intravenous infection with ten 50% animal infectious doses of the cell-free homologous virus. The challenge dose of this SIVmac251 virus stock had previously caused persistent infection in all (21 of 21) nonimmunized controls. A plasma pool was obtained from a donor that had been immunized with an inactivated whole SIVmac251 vaccine produced in human T cells. This plasma pool contained low levels of SIVmac binding and neutralizing antibody but had a high titer of antibodies recognizing human cell proteins. Given 4 or 18 hr before intravenous challenge, this plasma completely protected three of eight recipients from infection and delayed virus detection in one recipient. The five unprotected animals had only a transient or undetectable p27 antigenemia and low virus load in their PBMCs, and all survived at least 7 months after infection. By contrast, no protection was observed in 6 monkeys given inactivated, pooled plasma or purified immunoglobulin (Ig) from healthy SIVmac251-infected animals. This plasma pool and the Ig preparation contained high levels of SIV-binding and neutralizing antibody but no reactivity to human cellular components. Five of the six recipients had persistent antigenemia after challenge and four died acutely from
simian AIDS
in 4-7 months. These studies suggest that passive transfer of antibody to human cellular antigens can confer protection against SIVmac whereas passive transfer of neutralizing antibodies without human cellular antibodies does not protect against the homologous virus and may enhance infection.
...
PMID:Passive immunization of rhesus macaques against SIV infection and disease. 754 12
Mycobacterium avium complex (MAC) in simian
immunodeficiency
virus (SIV)-infected macaques is a frequent opportunistic infection that shares many features with the condition in human AIDS patients. A retrospective analysis of necropsies on 135 macaques with SIV-induced
simian AIDS
that received neither antiretroviral nor antimicrobial therapy revealed that 17% (23/135) were infected with MAC. MAC developed in 31.3% (21/67) of the animals inoculated with uncloned SIVmac251 versus 1.9% (1/53) and 6.7% (1/15) of the animals inoculated with the molecular clones SIVmac239 and SIVmac239/316EM, respectively (P = .001). This is the first example in which the risk of infection with a specific opportunistic organism was affected by the infecting strain of
immunodeficiency
virus. In addition, animals with MAC had a longer mean survival after primary infection and lower CD4 cell counts at death than animals that did not develop this opportunistic infection. The SIV-inoculated macaque is a valuable model in which to study the pathogenesis of MAC in the immunocompromised host.
...
PMID:Mycobacterium avium complex in macaques with AIDS is associated with a specific strain of simian immunodeficiency virus and prolonged survival after primary infection. 756 Dec 1
Proliferative lesions were found on the squamous epithelium of the tongue, esophagus, or penis or haired skin of the lip, hand, or thorax of 8 simian
immunodeficiency
virus-infected rhesus monkeys that died of
simian AIDS
. The lesions were focal and consisted of hyperkeratosis, parakeratosis, and acanthosis in the skin, with additional ballooning degeneration in the tongue, esophagus, and penis. The epithelial surfaces were frequently colonized by Candida species or gram-positive cocci. Intranuclear inclusion bodies were seen in cells in the middle and superficial layers. Herpesvirus virions were found in inclusion-bearing cells by transmission electron microscopy. An Epstein-Barr-like virus was identified in inclusion-bearing cells by immunohistochemistry and in situ hybridization. No virus was detectable in basal layers of the epithelium. These lesions resemble oral hairy leukoplakia in AIDS patients and may thus provide a useful primate model to study permissive epithelial infection by Epstein-Barr-like viruses.
...
PMID:Squamous epithelial proliferative lesions associated with rhesus Epstein-Barr virus in simian immunodeficiency virus-infected rhesus monkeys. 762 99
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