Vaccinia virus proteins on the plasma membranes of infected cells II. Expression of viral antigens and killing of infected cells by vaccinia virus-specific cytotoxic T cells

Abstract

Evidence is presented that virion-derived antigens as well as viral antigens expressed on cell surfaces after infection, may participate in the formation of “target-antigen complexes” (TACs) which render vaccinia virus-infected cells susceptible to recognition and killing by syngeneic, vaccinia virus-specific cytotoxic T cells (VV-CTLs). By employing L cells infected with trypsin-treated and untreated virions, evidence was obtained that proteins with molecular weights of 32K and 37K may be among the virion-derived antigens which participate in TAC formation. Following virus infection, a sequential expression of virus-specified antigens on the plasma membrane of infected cells could be detected. At 1 hr p.i., polypeptides with molecular weights of 48K–50K and 36K–37K were present on infected cell surfaces; by 2 hr p.i., polypeptides with molecular weights of 48K–50K, 42K–44K, 36K–37K, 29K–30K, and 16K–17K were detected on plasma membranes. As measured by in vitro, 51Cr-release assays, vaccinia virus-infected L cells were completely susceptible to lysis by VV-CTLs (⩾50% measured specific lysis) when (a) “early” but not late viral functions were expressed as measured with virus-infected cells which had been treated with hydroxyurea (5 X 10 −3, M) to block DNA replication or (b) when active protein synthesis was allowed to proceed for 90 min postadsorption and the infected cells were then treated with cycloheximide (100 μg/ml) to block further protein synthesis. Under these experimental conditions, polypeptides with molecular weights of 58K, 48K–50K, 42K, 36K–37K, 34K, 32K–33K, 27K–29K, and 16K–17K were expressed on the plasma membranes of vaccinia virus-infected cells but not uninfected cells. Whether each of the virion-derived and (or) virus-encoded polypeptides can associate with Class I, major histocompatibility antigens on the surfaces of virus-infected cells to form a primary or cross-reacting TAC recognized by VV-CTLs remains to be investigated.