Lentiviral encephalitides in the immature host: A comparison of human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus (SIV) brain infection
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The thymus is responsible for de novo production of CD4(+) and CD8(+) T cells and therefore is essential for T-cell renewal. The goal of this study was to assess the impact of simian immunodeficiency virus (SIV) infection on the production of T cells by the thymus. Levels of recent thymic emigrants within the peripheral blood were assessed through quantification of macaque T-cell receptor excision circles (TREC). Comparison of SIV-infected macaques (n = 15) to uninfected macaques (n = 23) revealed stable or increased TREC levels at 20 to 34 weeks postinfection. Further assessment of SIV-infected macaques (n = 4) determined that TREC levels decreased between 24 and 48 weeks postinfection. Through the assessment of longitudinal time points in three additional SIVmac239-infected macaques, the SIV infection was divided into two distinct phases. During phase 1 (16 to 30 weeks), TREC levels remained stable or increased within both the CD4 and CD8 T-cell populations. During phase 2 (after 16 to 30 weeks), TREC levels declined in both T-cell populations. As has been described for human immunodeficiency virus (HIV)-infected patients, this decline in TREC levels did at times correlate with an increased level of T-cell proliferation (Ki67(+) cells). However, not all TREC decreases could be attributed to increased T-cell proliferation. Further evidence for thymic dysfunction was observed directly in a SIVmac239-infected macaque that succumbed to simian AIDS at 65 weeks postinfection. The thymus of this macaque contained an increased number of memory/effector CD8(+) T cells and an increased level of apoptotic cells. In summary, reduced levels of TREC can be observed beginning at 16 to 30 weeks post-SIV infection and correlate with changes indicative of dysfunction within the thymic tissue. SIV infection of macaques will be a useful model system to elucidate the mechanisms responsible for the thymic dysfunction observed in HIV-infected patients.
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Infection with human immunodeficiency virus (HIV) commonly results in neurologic disease called the AIDS dementia complex. Neuronal loss and injury have been found in the HIV brain, but the underlying mechanisms are not understood. The simian immunodeficiency virus (SIV)–infected macaque is an excellent animal model for HIV infection, but neuronal loss has not been demonstrated. To determine whether neuronal damage occurs in the SIV brain, we quantified the neuronal markerN-acetylaspartate(NAA) using proton magnetic resonance spectroscopy (1H-MRS) in brain extracts of control and SIV-infected macaques and correlated these findings with histologic analyses. We found reduced NAA in the SIV-infected animals compared with controls (2.94 ± 1.37 versus 6.21 ± 1.73 µmol/g of wet weight; p = 0.004). A significant decrease in NAA was also found in SIV-infected animals sacrificed in the acute stages of infection 9 or 10 days after inoculation with SIV mac Ynef. We conclude that SIV infection of rhesus macaques results in neuronal damage that is demonstrable shortly after infection and that 1H-MRS may be used to measure such injury. The results further support the SIV macaque as a useful model to study the mechanisms of neuropathogenesis by HIV.
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Abstract: 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.
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The striking similarities between simian immunodeficiency virus (SIV)-induced disease in macaque monkeys and HIV-induced disease in humans make the SIV-induced macaque monkey an extraordinarily important model for the study of AIDS. The most significant difference between these lentivirus-induced syndromes is the more rapid progression of disease in SIV-infected monkeys. The immunologic and pathologic manifestations of SIV infections in rhesus monkeys are described.
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Tripartite motif 5α (TRIM5α) is a potent antiretroviral immune factor present in the cytoplasm of cells of most tissue types. The rhesus macaque TRIM5 gene has been shown to display polymorphism, with different variants being divided into three groups (TRIM5 TFP , TRIM5 Q , and TRIM5 CypA ), which may have divergent retroviral effects on infection. Along with rhesus macaques, cynomolgus macaques are also used in simian immunodeficiency virus (SIV) infection studies. As a consequence, TRIM5 genotyping of these animals will contribute to interpreting the outcome of such studies. The present communication covers Burmese, Chinese, and a large cohort of Indian‐origin rhesus macaques, and describes the first large cohort study on TRIM5 polymorphism in outbred cynomolgus macaques. We demonstrate the presence of the TRIM5 TFP group in cynomolgus macaques. In addition, we have re‐evaluated historical samples of rhesus macaques challenged with SIV mac251 , a virus that has been reported to be partially suppressed by particular rhesus macaque TRIM5 variants.
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It is well established that HIV infection can lead to motor/cognitive disorders in humans. A number of studies have shown that simian immunodeficiency virus (SIV) infection in rhesus macaques parallels many aspects of HIV disease in humans. The purpose of this study was to define further the SIV-infected rhesus macaque as a model of neuro-AIDS. Our objective was to detect movement-related impairments in behaviorally trained, SIV-infected macaques using both simple and choice reaction time tasks. Reaction times (RTs), movement times (MTs), and error types were examined. Nine monkeys were infected with neurovirulent strains of SIVmac, four of which served initially as controls before their inoculation. Seven of the nine monkeys developed simian AIDS within 4 months of inoculation (rapid progressors), while two monkeys survived for more than 1 year postinoculation (slow progressors). Of the rapid progressors, four exhibited slowed reaction times and six showed movement time slowing. One rapid progressor showed evidence of a strategy shift to overcome impaired motor abilities. Monkeys with rapidly progressing SIV-related disease consistently show behavioral abnormalities reflecting underlying neuronal injury. Although the slow progressors also showed RT and/or MT slowing, a role for nonspecific factors related to late-stage simian AIDS could not be ruled out in these cases. The results demonstrate that motor impairments associated with SIV infection in rhesus macaques can be detected using RT and MT measures, further establishing the SIVmac-infected macaque monkey as a viable model of neuro-AIDS.
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