SUMMARYThe uptake of two forms of Trichoplusia ni multiple nucleocapsid nuclear polyhedrosis virus by SpodopleraJrugiperda cells in culture has been evaluated. Subtle differences in the Mg 2+ and Ca 2+ requirements for the uptake of cell-released virus (CRV) and polyhedron-derived virus (PDV) exist; otherwise, both forms of the virus appeared similar in their mode of uptake. Entry occurs by fusion of the plasma membrane of the cell with the envelope surrounding the virus nucleocapsid at neutral pH. The receptor turnover for the virus probably occurs rapidly since saturation of receptor sites for the virus was not achieved. The binding and penetration of the virus, and the uncoating and transport of the viral genome to the nucleus is rapid. Uncoating occurs predominantly in the cytoplasm. The lower infectivity of PDV, compared with CRV, for cells in culture may happen because this form of the virus accumulates in cell vacuoles and is unable to proceed with infection.

SUMMARY[E]-5-(2-bromovinyl)-2'-deoxyuridine (BVdU) inhibits the replication of the baculovirus Trichoplusia ni multiple nucleocapsid nuclear polyhedrosis virus in Spodoptera frugiperda cells. Virus-specific DNA synthesis and late protein synthesis are suppressed by the drug. BVdU is phosphorylated by deoxythymidine (deoxycytidine) kinase present in both uninfected and virus-infected cells, and in its 5'-triphosphate form it inhibits DNA polymerase activity in virus-infected cells. The effect of the BVdU is not completely reversible. Phosphonoacetic acid, phosphonoformic acid and Acyclovir have no effect on baculovirus replication. Acyclovir fails to compete with deoxycytidine and thymidine as substrates for pyrimidine deoxynucleoside kinase in virus-infected and uninfected cells.