In this study, ivermectin was found to be ineffective for prevention of a lethal infection with the Senegal strain of Zika virus in Ifnar1 knockout mice.
Taken together, our observations suggest that ZIKV infection induces a type I IFN response via RLRs and that ZIKV interferes with this response by blocking signaling downstream of RLRs and IFNAR.
Two common immunocompromised mouse strains used in transmission studies-male with genes encoding interferon types I and II receptor gene knockout (IFNAR/IFNGR; AG129) and with interferon type 1 receptor knockout (Ifnar<sup>-/-</sup>) were infected with a Puerto Rican Zika virus isolate (PRVABC59), and pathology was assessed 5 to 11 days after infection.
Here, we investigate the neuropathogenesis of ZIKV infection in type I interferon receptor IFNAR knockout (Ifnar1 <sup>-/-</sup> ) mice, an infection model that exhibits high viral burden within the central nervous system.
Here, we show that DENV-immune Ifnar1 <sup>-/-</sup> or wild-type C57BL/6 mice infected with ZIKV have cross-reactive immunity to subsequent ZIKV infection and pathogenesis.