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

The macaque infectious dose (MID) of a single-cell clone of simian immunodeficiency virus isolated from a pig-tailed macaque (SIV/Mne clone E11S) was determined in rhesus macaques (Macaca mulatta). Twenty-one macaques were inoculated with 10-fold dilutions of the virus stock (three or four animals per dose). The virologic and clinical status of these animals was monitored for 26 weeks. The 25% MID (MID25) occurred at a 10(5)-fold dilution of the viral stock.
J Med Primatol
PMID:Infectivity of titered doses of simian immunodeficiency virus clone E11S inoculated intravenously into rhesus macaques (Macaca mulatta). 796 38

The presence of sperm in testicular tissue of rhesus macaques that died as a result of infection with simian immunodeficiency virus (SIV) was related to age and body weight. Depressed testosterone levels were not associated with elevated LH levels. The data suggest that azoospermia in the SIV-infected macaques was due to cachexia and not a direct effect of virus on the testis, supporting a similar hypothesis regarding azoospermia in men infected with human immunodeficiency virus.
J Med Primatol 1993 Jul
PMID:Spermatogenesis and hormone levels in rhesus macaques inoculated with simian immunodeficiency virus. 828 23

The lineage of HIV-2-like viruses was studied in feral sooty mangabeys (SMs) by serological and genetic methods. Four feral sooty mangabeys were positive for simian immunodeficiency virus (SIV) antibodies and a new isolate, SIVsmSL92a, was obtained. Genetic analysis of gag genes showed that SIVsmSL92a was highly diverse and a distinct sequence subtype within the SIV sm/HIV-2 family. The results showed that SIVsm is the most diverse group of SIVs found thus far in a single monkey species.
J Med Primatol 1995 May
PMID:Isolation and characterization of the first simian immunodeficiency virus from a feral sooty mangabey (Cercocebus atys) in West Africa. 875 Oct 49

A cohort of rhesus macaques (Macaca mulatta), obtained from the California Regional Primate Research Center (CRPRC) and necropsied in 1970-72 with lesions suggestive of simian immunodeficiency virus (SIV) infection, was identified at the New England Regional Primate Research Center (NERPRC). Polymerase chain reaction (PCR), DNA sequence analysis, and in situ hybridization were used to confirm the presence of SIV nucleic acids. This represents the earliest case of SIV infection at the NERPRC and suggests a common source for present day SIV isolates.
J Med Primatol 1995 May
PMID:Origins of simian immunodeficiency virus infection in macaques at the New England Regional Primate Research Center. 875 Oct 50

This study reports on the endothelial expression of vascular cell adhesion molecule-1 (VCAM-1) in the central nervous system (CNS) early after experimental infection of rhesus monkeys (Macaca mulatta) with pathogenic and nonpathogenic simian immunodeficiency virus (SIV). Diffuse endothelial expression of VCAM-1 was observed in the CNS in all animals receiving pathogenic SIV. These findings demonstrate the rapidity with which pathogenic SIV is able to enter the CNS and induce endothelial cell activation.
J Med Primatol 1995 May
PMID:VCAM-1 expression and leukocyte trafficking to the CNS occur early in infection with pathogenic isolates of SIV. 875 Oct 51

Retrospective data indicate that two separate outbreaks of simian AIDS and associated lymphoma were caused by Simian Immunodeficiency Virus (SIVmac and SIVstm, respectively) in group-housed macaques at the California Regional Primate Research Center (CRPRC) in the early and mid-1970s. Because these epizootics were not then recognized as infectious in nature, surviving healthy SIV carriers were sent to other primate centers where they transmitted the viruses to resident macaques. The source of SIV at the CRPRC was by contact with co-housed seropositive sooty mangabeys. Spread of SIV via saliva and blood while fighting most likely accounted for these epizootics. Separate outbreaks of a somewhat different version of simian AIDS, caused by the simian Type D retrovirus (SRV-1), and spread from healthy carriers via saliva and blood also occurred in the late 1970s and early 1980s in group-housed macaques at the CRPRC. Initially, these SRV-1 outbreaks were also not recognized as infectious.
J Med Primatol 1996 Jun
PMID:The history of simian AIDS. 889 35

Research on human immunodeficiency virus (HIV) infection is compromised by the obvious limitation in having for study only virus-infected individuals or those exposed to the virus. Steps involved in transmission or pathogenesis require planned experimentation. The identification of animal models of acquired immunodeficiency syndrome (AIDS) has therefore been helpful for evaluating phases of HIV pathogenesis. Of the seven subgenera of lentiviruses now recognized, two share the characteristics with HIV of a T cell tropism and the associated loss of CD4+ cells in the host associated with disease: the feline immunodeficiency virus (FIV) and the simian immunodeficiency virus (SIV) (Table 1). The other animal lentiviruses grow best in macrophages and their infection generally reflects clinical sequellae of infection of this cell type. This review addresses those features of SIV, HIV, and SHIV infections of non-human primates that illustrate the importance of the animal models of AIDS.
J Med Primatol 1996 Jun
PMID:The value of primate models for studying human immunodeficiency virus pathogenesis. 889 37

We explored the relationship between T cell activation signals and dendritic cells (DC) in the replication cycle of immunodeficiency viruses. First we analyzed the effect of two cell cycle inhibitors (mimosine and aphidicolin) on SIV reverse transcription, circularization, and integration in macaque resting T cells stimulated with anti-CD3 mAb at the time of infection. The formation of SIV LTR circles was blocked by the G1 inhibitor mimosine. The G1/S inhibitor aphidicolin neither affected circularization nor integration of SIV DNA. Therefore, the induction of SIV LTR circle production is likely to be mediated by signaling events normally regulating the G1 to S transition. We further characterized DC-dependent HIV-expression in human T cells. We examined the effect of ligating two novel receptors, IPO-3 and Bgp95, on DC-dependent HIV-1 expression. Activation of DCs through IPO-3 receptors, and to a lesser extent Bgp95 ligation, upregulated HIV spread in these cells. The mechanisms by which IPO-3 vs. Bgp95 increase HIV-1 levels appear to be different. In particular, IPO-3 ligation alone on T cells also increased HIV-1 levels. Activation of T cells via defined surface receptors or with DCs is required for establishing HIV/SIV cDNA synthesis in T cells.
J Med Primatol 1996 Jun
PMID:Immunodeficiency virus cDNA synthesis in resting T lymphocytes is regulated by T cell activation signals and dendritic cells. 889 41

The larvae of Mesocestoides are rarely encountered in nonhuman primates, with most cases reported in baboons. Infection of macaques has been occasionally diagnosed, but Mesocestoides in the lung parenchyma is extremely rare. We have previously demonstrated that in macaques with terminal AIDS, simian immunodeficiency virus (SIV)-infected leukocytes are rarely found in cellular infiltrates associated with opportunistic infections or preexisting disease. Here we describe larvae (tetrathyridia) of the cestode Mesocestoides in the lung of an adult, pigtailed macaque (Macaca nemestrina) during acute SIV infection in which virus-positive cells are present within the cellular infiltrates. These results describe a rare parasitic disease in pigtailed macaques and demonstrate that lentivirus-infected leukocytes can be associated with inflammatory sites during acute infection.
J Med Primatol 1996 Aug
PMID:A case of pulmonary cestodiasis in a simian immunodeficiency virus-infected pigtailed macaque (Macaca nemestrina) in which virus-infected leukocytes are present within the lesion. 890 3

The primary mode of human immunodeficiency virus (HIV) transmission worldwide is by exposure to the virus at vaginal, rectal, and oral mucosal surfaces. To understand HIV/simian immunodeficiency virus (SIV) transmission events at mucosal portals of entry, we used the SIV-macaque model to determine if mucosal surfaces function as barriers and select for particular viral genotypes. Rhesus macaques were inoculated intravaginally, intracolonically, intrarectally, or orally with the complex primary viral isolate SIV/DeltaB670. Peripheral blood mononuclear cells, collected within the first two weeks postinoculation, were cloned and sequenced from all infected macaques. In the majority of the animals analyzed, multiple genotypes were identified, independent of the route of infection. These findings suggest that the mucosal barrier may play a minor role in the genotypic selection observed during sexual transmission of HIV and emphasize the need to evaluate the viral diversity present within the mucosal secretions of chronically infected individuals.
J Med Primatol
PMID:SIV/DeltaB670 transmission across oral, colonic, and vaginal mucosae in the macaque. 927 Nov 83


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