Abstract
In nature, primate lentiviruses infect humans and several Old World monkeys and apes. However, to date, lentiviruses infecting New World monkeys have not been described. We studied the susceptibility of common marmoset cells to HIV-1 infection and observed the presence of post-entry blocks to the early phase of HIV-1 infection in peripheral blood lymphocytes (PBLs) and a B lymphocytic cell line (B-LCL). The blocks present in these cells are dominant and phenotypically different from each other. In PBLs, the block occurs at the level of reverse transcription, reducing the accumulation of early and late transcripts, similar to the block imposed by TRIM5α. However, we have found that marmoset TRIM5α does not block HIV-1. In contrast, the restriction factor present in B-LCLs blocks HIV-1 replication at a later step, after nuclear entry, and inhibits integration. Additionally, we have identified an HIV-1 capsid mutant, N74D, that is able to escape the restriction in the marmoset B-LCLs. Our results suggest that the factors responsible for the blocks present in marmoset PBLs and B-LCLs are different. We propose the existence of at least two new restriction factors able to block HIV-1 infection in marmoset lymphocytes.
Highlights
New World monkeys are apparently resistant to infection by known lentiviruses
To investigate the presence of additional early blocks to HIV-1 infection in primary lymphocytes of common marmosets, we prepared single-cycle luciferase reporter viruses pseudotyped with the vesicular stomatitis virus G (VSV-G) envelope glycoprotein in 293T cells
The recombinant viruses used to test HIV-1 infectivity in peripheral blood lymphocytes (PBLs) were pseudotyped with VSV-G, which has been shown to mediate viral entry through clathrin-based endocytosis[16,17,18]
Summary
Some of the blocks to HIV-1 infection in common marmosets, a New World monkey, have been characterized. Common marmoset A3G and BST2 block HIV-1 replication[14]. Using a directed evolution method that takes advantage of the natural ability of the virus to mutate during replication, we have generated HIV-1 variants able to replicate in cells expressing common marmoset CD4 and CXCR415, A3G or BST214. We report the existence of two additional post-entry blocks in common marmoset primary lymphocytes and a B lymphocytic cell line (B-LCL). This work provides new insights into virus-host interactions. Understanding how these restriction factors operate and how the virus is able to escape from these blocks in different species could assist the development of novel interventions against HIV-1 infection
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