Due to an error in manuscript preparation, an incorrect shRNA sequence for IRS2 was published. The correct hairpin sequence is a 19-nt stretch beginning from nt 703 of the published IRS2 cDNA sequence (XM_357863). The oligonucleotides cloned into the U6 construct for the IRS2U6 adenovirus are as follows: tcgagGTGACGCTGCAGCTTATGAttcaagagaTCATAAGCTGCAGCGTCACttttt (forward) and ctagAAAAAGTGACGCTGCAGCTTATGAtctcttgaaTCATAAGCTGCAGCGTCACc (reverse). In addition, the shRNA cassettes were cloned into the adenoviral cosmid pAxcwit, which lacks a promoter, and not the cosmid pAxCAwtit, as published..The authors regret this error.

Natural SIVmnd and STLVmnd infections of mandrills in a colony at the Centre International de Recherches Médicales de Franceville (CIRMF) in Gabon were investigated by genetic analysis to determine the extent of intracolony transmission. SIVmnd pol sequence analysis indicates that the six strains present in the colony belong to the SIVmnd lentivirus subgroup previously defined according to the only available prototype sequence (SIVmndGB1), which originated from the same colony. The intraanimal nucleotide diversity (1.1-3.1%) was similar in range to that reported in individuals infected by other HIV/SIVs. The interanimal diversity (0.5-4.3%) was not significantly different from that observed in each individual mandrill, indicating an epidemiological link among the SIVmnd isolates of distinct animals within the colony. Phylogenetic analysis of these isolates, together with seroepidemiological and behavior surveillance within the colony, indicates a predominant male-to-male transmission of SIVmnd that probably occurred during bouts of interanimal aggression. Moreover, our results suggest one case of vertical transmission of SIVmnd from a naturally infected founder female to one of her six offspring. The first genetic analysis of STLV isolates from mandrills is also reported here. Partial tax/rex sequences were used to evaluate the diversity between seven STLVmnd isolates and their phylogenetic relationships with other known strains of human and nonhuman primate T cell leukemia virus, types I and II (PTLV-I/II). They all belong to the PTLV-I subtype, but two genetically distinct STLVmnd groups were evidenced within the mandrill colony. The phylogenetic analyses of the STLVmnd isolates, together with seroepidemiological and behavior surveillance of the mandrills, indicate that intracolony transmissions of STLVmnd are also predominantly the result of male-to-male aggressive contacts.

T cell activation levels in HIV infection are predictive of AIDS progression. We searched for the immunological correlates of protection against disease progression by studying the early stages of nonpathogenic SIV infection in African green monkeys (SIVagm). The African green monkeys (AGMs) displayed high peak viremias and a transient decline in levels of blood CD4 + and CD8 + T cells between days 5 and 17 after infection. A concomitant increase in levels of CD4 + DR + , CD8 + DR + , and CD8 + CD28 -cells was detected. After the third week, T cell activation returned to baseline levels, which suggested a protective downregulation of T cell activation. A very early (24 hours after infection) and strong induction of TGF-β1 and FoxP3 expression was detected and correlated with increases in levels of CD4 + CD25 + and CD8 + CD25 + T cells. This was followed by a significant increase in levels of IL-10, whereas IFN-γ gene upregulation was more transient, and levels of TNF-α and MIP-1α/β transcripts did not increase in either blood or tissues. The profiles were significantly different during primary SIV infection in macaques (SIVmac); that is, there was a delayed increase in IL-10 levels accompanied by moderate and persistent increases in TGF-β levels. Together, our data show that SIVagm infection is associated with an immediate antiinflammatory environment and suggest that TGF-β may participate in the generation of Tregs, which may prevent an aberrant chronic T cell hyperactivation.

Among the primates held at the CIRMF Primate Center, Gabon, no serological sign of SIV infection could be demonstrated in 68 cynomolgus monkeys, 60 chimpanzees, nine gorillas, and 12 sun-tailed monkeys, while seven of 102 mandrills and six of 24 vervets were infected with SIV. Six mandrills, seven vervets and ten cynomolgus monkeys exhibited a full HTLV type 1 Western blot profile. The sera of two gorillas and one chimpanzee presented with a positive but not typical HTLV Western blot profile. The sera of the gorillas lacked p24 antibodies, and the chimpanzee had a Western blot profile evocative of HTLV-II. All attempts to amplify viruses from these animals by PCR were unsuccessful. Two other chimpanzees and seven gorillas presented with indeterminate HTLV Western blot profiles. In the mandrill colony, only male animals were STLV seropositive and no sexual transmission to females was observed. SIV infection was also more frequent in male than female mandrills and sexual transmission appeared to be a rare event. No SRV infection was observed in macaques.

Due to an error in manuscript preparation, an incorrect shRNA sequence for IRS2 was published. The correct hairpin sequence is a 19-nt stretch beginning from nt 703 of the published IRS2 cDNA sequence (XM_357863). The oligonucleotides cloned into the U6 construct for the IRS2U6 adenovirus are as follows: tcgagGTGACGCTGCAGCTTATGAttcaagagaTCATAAGCTGCAGCGTCACttttt (forward) and ctagAAAAAGTGACGCTGCAGCTTATGAtctcttgaaTCATAAGCTGCAGCGTCACc (reverse). In addition, the shRNA cassettes were cloned into the adenoviral cosmid pAxcwit, which lacks a promoter, and not the cosmid pAxCAwtit, as published..The authors regret this error.