Some studies have suggested that people with HIV may respond less well to vaccines against SARS-CoV-2. We comprehensively compared B- and T-cell responses to different COVID-19 vaccines in middle-aged persons with well-treated HIV and individuals of the same age without HIV, who were also highly comparable in terms of demographics and lifestyle, including those with prior SARS-CoV-2 infection.

The mitochondrial antiviral protein MAVS is a key player in the induction of antiviral responses; however, human immunodeficiency virus 1 (HIV-1) is able to suppress these responses. Two linked single nucleotide polymorphisms (SNPs) in the MAVS gene render MAVS insensitive to HIV-1-dependent suppression, and have been shown to be associated with a lower viral load at set point and delayed increase of viral load during disease progression. Here, we studied the underlying mechanisms involved in the control of viral replication in individuals homozygous for this MAVS genotype. We observed that individuals with the MAVS minor genotype had more stable total CD4+ T cell counts during a 7-year follow up and had lower cell-associated proviral DNA loads. Genetic variation in MAVS did not affect immune activation levels; however, a significantly lower percentage of naïve CD4+ but not CD8+ T cells was observed in the MAVS minor genotype. In vitro HIV-1 infection of peripheral blood mononuclear cells (PBMCs) from healthy donors with the MAVS minor genotype resulted in decreased viral replication. Although the precise underlying mechanism remains unclear, our data suggest that the protective effect of the MAVS minor genotype may be exerted by the initiation of local innate responses affecting viral replication and CD4+ T cell susceptibility.

Sexual transmission is the major route of HIV-1 infection worldwide. The interaction of HIV-1 with mucosal dendritic cells (DCs) might determine HIV-1 susceptibility as well as initial antiviral immunity controlling virus in the chronic phase. Different DC subsets reside in mucosal tissues and express specific C-type lectin receptors (CLRs) that interact with HIV-1 with different outcomes. HIV-1 has been shown to subvert CLRs for viral transmission and immune evasion, whereas CLRs can also protect against HIV-1 infection. Here, we will discuss the role of CLRs in HIV-1 transmission and adaptive immunity, and how the CLRs dictate the function of DCs in infection. Ultimately, understanding the interplay between CLRs and HIV-1 will lead to targeted approaches in the search for preventative measures.