ArticlemBio2026
Repression of productive viral replication by KSHV LANA correlates with reduced adaptive immune activation: potential implications for KSHV immune evasion.
Article in mBio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Adaptive immune responses to primary Kaposi sarcoma-associated herpesvirus (KSHV) infection are poorly defined. To develop better small-animal models for understanding KSHV pathogenesis and immunity, we previously generated a chimeric virus in which the KSHV latency-associated nuclear antigen (kLANA), a conserved multifunctional protein critical for viral latency, was exchanged for the LANA homolog in murine gammaherpesvirus 68 (MHV68). Despite supporting comparable levels of latent infection between wild-type (WT) and KLKI MHV68, kLANA directly repressed MHV68 lytic replication and reactivation. We therefore hypothesized that suppression of lytic replication by kLANA dampens adaptive immune responses. To test this, mice were infected with equivalent doses of either WT or KLKI MHV68, and adaptive immune responses were evaluated over time. Compared to the WT virus, polyclonal B and T cell activation was starkly reduced following KLKI MHV68 infection, which correlated with reduced virus-specific humoral immunity and effector CD4
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