Infection Of African Monkeys Research Articles

Antiretroviral Therapy in Simian Immunodeficiency Virus-Infected Sooty Mangabeys: Implications for AIDS Pathogenesis.

Simian immunodeficiency virus (SIV)-infected sooty mangabeys (SMs) do not develop AIDS despite high levels of viremia. Key factors involved in the benign course of SIV infection in SMs are the absence of chronic immune activation and low levels of infection of CD4(+) central memory (TCM) and stem cell memory (TSCM) T cells. To better understand the role of virus replication in determining the main features of SIV infection in SMs, we treated 12 SMs with a potent antiretroviral therapy (ART) regimen for 2 to 12 months. We observed that ART suppressed viremia to <60 copies/ml of plasma in 10 of 12 animals and induced a variable decrease in the level of cell-associated SIV DNA in peripheral blood (average changes of 0.9-, 1.1-, 1.5-, and 3.7-fold for CD4(+) transitional memory [TTM], TCM, effector memory [TEM], and TSCM cells, respectively). ART-treated SIV-infected SMs showed (i) increased percentages of circulating CD4(+) TCM cells, (ii) increased levels of CD4(+) T cells in the rectal mucosa, and (iii) significant declines in the frequencies of HLA-DR(+) CD8(+) T cells in the blood and rectal mucosa. In addition, we observed that ART interruption resulted in rapid viral rebound in all SIV-infected SMs, indicating that the virus reservoir persists for at least a year under ART despite lower infection levels of CD4(+) TCM and TSCM cells than those seen in pathogenic SIV infections of macaques. Overall, these data indicate that ART induces specific immunological changes in SIV-infected SMs, thus suggesting that virus replication affects immune function even in the context of this clinically benign infection. Studies of natural, nonpathogenic simian immunodeficiency virus (SIV) infection of African monkeys have provided important insights into the mechanisms responsible for the progression to AIDS during pathogenic human immunodeficiency virus (HIV) infection of humans and SIV infection of Asian macaques. In this study, for the first time, we treated SIV-infected sooty mangabeys, a natural host for the infection, with a potent antiretroviral therapy (ART) regimen for periods ranging from 2 to 12 months and monitored in detail how suppression of virus replication affected the main virological and immunological features of this nonpathogenic infection. The observed findings provide novel information on both the pathogenesis of residual immunological disease under ART during pathogenic infection and the mechanisms involved in virus persistence during primate lentiviral infections.

Characterization of an antigen-antibody system associated with epidemic non-A,non-B hepatitis in west africa and experimental transmission of an infectious agent to primates

Summary An epidemic of non-A, non-B hepatitis (NANBH) was studied in Tortiya, Ivory Coast, over a period of 17 months. Highly sensitive serologic tests performed on serum samples from patients with this type of hepatitis excluded both HAV (hepatitis A virus) and HBV (hepatitis B virus) as aetiologic agents. The mode of spread of the epidemic, clinical features and frequent cases of fulminant hepatitis in pregnant women resembled that of other recently described water-borne outbreaks of non-A,non-B hepatitis. Oral-faecal transmission of this form of NANBH was shown by experimental infection of African monkeys, which developed antibody of the IgM class specifically reacting with the antigen present in stools of infected persons. Using the immunoenzymatic test employing monkey IgM on solid phase and enzyme-labelled IgG purified from sera of patients convalescing from NANBH, we identified the antigen associated with the possible causative NANBH agent. These data confirm the existence of a distinct human NANBH agent responsible for epidemic out-breaks of NANBH. This agent is different from those of the postransfusion type of NANBH and antigenically unrelated to HAV. The direct serologic test presented here may be useful for diagnosis of an epidemic form of NANBH.