AIDS in child ren ." Some ha ve suggested that PLH and LIP represent a spe ctru m of lymphoid lesions in ped iatric AIDS and may be related to infe ction with Epstei n-Ba rr vi ru s (EBV ).21 SIV infection occurs spontaneously and asymptomati cally in African green monkeys (Cercopithecus aethiopsv?and mangabey monkeys (Cercocebus atys).16.29 When macaques ar e acc id entally or expe rime ntally infected with SIV th ey dev elop an immunodeficien cy sy n d r o me that shares m an y features with AIDS. 2.4.5.8.1 4.24.27 Pulmonary lesions associated with o ppo rt un istic agents ha ve been described in SIV -infect ed rh esus m onkeys' r'> and pulmonary multinucleat e giant cell and hi stiocyt ic infiltrate s have been mentioned ,3,22.25,27 but th e pulmonary changes specificall y due to SIV infection ha ve not been pre viously reported in detail. We describ e pulmonary lesions in SIV-infected rhe sus monkeys that appear to be directly due to SIV. Abstract. Necropsy reports from 28 rhesus monkeys that had been experimentally infected with simian immun odeficiency virus (SIV) and that were free of cytomegalovirus were reviewed. Lung sections from 24 of these monkeys that had no etiologic agent other than SIV detected in the lung were studied in detail by histopath ologic, immun ohistochemical, and electron microscopic examination and by in situ hybridization. Fourt een of the monkeys were part of a serial euthanasia study, while others were euthanatized after they became moribund. The following lesions were detected: perivascular inflammation, vasculitis, interstitial pneumonia, syncytial cells, hemorrhage, fibrin exudation, and pleural fibrosis. Perivascular inflamm ation was the most frequent lesion and occurred as early as 2 weeks after inoculation. Severe pneumonia and numerous syncytial cells were seen only in animals euthanatized because they had become moribund . The lesions appeared to be directly due to SIV infection. SIV antigens, RNA, and virions were detected in syncytial cells and macrophages by immunohistochemical examination, in situ hybridization, and transmission electron microscopic examination, respectively. The amount of virus present was correlated with the severity of the lesions. The SIVinduced lesions were different from those of the lymphocytic interstitial pneumonia, which occurs in human immunodeficie ncy virus-infected children and in ovine lentivirus-infected sheep and goats.Key words: Simian immun odeficiency virus; lung; pneumonia; Rhesus monkeys.Lentiviruses, a subfa m ily of retroviruses, include th e human immunodeficiency viruses (HIV), simian immunod eficiency viru ses (SIV) , equin e infectious an emia virus (EIAV), ovine lentiviruses (OvLV), bo vine immunodeficiency-like virus, and felin e immunodeficiency virus. As a group, lentiviruses cause chronic infections and a variety of dis ease syndromes, such as immunodeficien cy, encephalitis, pn eumonia, arthritis, an emia, thrombocytopenia, and lymphoid hyp erplasia. HIV-infected human beings with th e acquired immunodeficiency sy...

Eradication of human immunodeficiency virus 1 (HIV-1) from an infected individual cannot be achieved using current antiretroviral therapy (ART) regimens. Viral reservoirs established in early infection remain unaffected by ART and are able to replenish systemic infection upon treatment interruption. Simian immunodeficiency virus (SIV) infected macaque models are useful for studying HIV pathogenesis, treatments, and persistent viral reservoirs. Here, we used the SIV macaque model to examine and quantify RNA and DNA positive cells in tissues from macaques that control viral replication (controllers) and those that have persistently high plasma viremia (progressors). A positive correlation was detected between tissue RNA+ cells and plasma viral load in both mesenteric lymph node (LN) and spleen. Similarly, a positive correlation also observed between DNA+ cells and plasma viral load in ileum and jejunum. Controllers had a lower frequency of both RNA and DNA+ cells in several tissues compared to progressors. However, DNA+ cells were prevalent in mesenteric LN, inguinal LN, colon, midbrain, and bone marrow tissues in both controller and progressors. Organized lymphoid tissues of LNs, spleen, and intestine were found as the major tissues positive for virus. Viral RNA and DNA positive cells were detected in brain and thymus in macaques with high plasma viremia and SIV-encephalitis. Both T cells and macrophages were shown to be infected in several tissues, indicating vaccines and ART should be specifically designed to protect these cells in organized lymphoid tissues. These results indicate ART should target infected cells in secondary lymphoid organs to reduce both productively and latently infected cells.

Identifying the cells that can be infected with HIV in vivo, and thus potentially persist as latent reservoirs is of high priority. Here, we report the major infected cells in a chronically-SIV infected macaque that developed AIDS and encephalitis. Majority of the infected cells were detected as non-proliferating resting cells. SIV infected non-proliferating resting cells were found to be playing an important role in viral pathogenesis, persistence or reservoir formation.