In addition, IFN-I signaling was significantly up-regulated with the viral replication, and was higher in the stHIV-1sv infected macaques. Compared to the HIV-1 NL4−R3A, stHIV-1sv showed a notably higher level of replication, and the NPMs infected with the latter induced a more robust neutralizing antibody but a weaker cellular immune response. HIV-1 NL4−R3A and stHIV-1sv can replicate persistently in NPMs during 41 weeks of acute infection stage. To optimize HIV-1 infection in NPMs therefore, we generated HIV-1 NL4−R3A and stHIV-1sv, and infected NPMs with these viruses. However, the HIV-1-infected NPMs showed relatively high viremia in the first 6 weeks of infection, which declined thereafter suggesting that HIV-1 NL4−3 infection in these animals was only partly permissive. In our previous study, we demonstrated that HIV-1 NL4−3 successfully infected NPMs and formed a long-term viral reservoir in vivo.
The northern pig-tailed macaques (NPMs) lack TRIM5α, an antiviral restriction factor, and instead have TRIM5-CypA.
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