(1996). A titration procedure of the Junonia coenia densovirus and quantitation of transfection by its cloned genomic DNA in four lepidopteran cell lines.
(2007). ArmasPortela R: Productive entry of type C foot-and-mouth disease virus into susceptible cultured cells requires clathrin and is dependent on the presense of plasma membrane cholesterol. Virology
(2008). Balasuriya UBR: Persistent equine arteritis virus infection in HeLa cells.
(2006). Belsham GJ: Role of RNA structure and RNA binding activity of Foot-and-Mouth disease virus 3C protein in VPg uridylylation and virus replication.
(1987). Blaas D: Mechanism of entry of human rhinovirus 2 into HeLa cells. Virology
(1983). BN: Ammonium chloride prevents lytic growth of reovirus and helps to establish persistent infection in mouse L cells. Science
(1993). BN: Cells and viruses with mutations affecting viral entry are selected during persistent infections of L cells with mammalian reoviruses.
(2009). C: A novel single-cell quantitative real-time RT-PCR method for quantifying foot-and-mouth disease viral RNA. J Virol Methods
(1985). Coevolution of cells and virus as a mechanism for the persistence of lymphotropic minute virus of mice in L-cells.
(1998). Colbère-Garapin F: Molecular mechanisms of poliovirus persistence: key role of capsid determinants during the establishment phase. Cell Mol Life Sci
(2000). Cytopathogenesis and inhibition of host gene expression by RNA viruses. Microbiol Mol Biol R
(2009). Development and validation of a duplex quantitative real-time RT-PCR assay for simultaneous detection and quantitation of foot-and-mouth disease viral positive-stranded RNAs and negative-stranded RNAs.
(1993). Distinctive features of foot-and-mouth disease virus, a member of the picornavirus family: aspects of virus protein synthesis, protein processing and structure. Prog Biophys Mol Bio
(2005). DL: Comparative genomics of foot-and-mouth disease virus.
(1988). E: Coevolution of cells and viruses in a persistent infection of foot-and-mouth disease virus in cell culture.
(1985). E: Establishment of cell lines persistently infected with foot-and-mouth disease virus. Virology
(1994). E: Rapid cell variation can determine the establishment of a persistent viral infection.
(1987). Effect of lysosomotropic compounds on early events in foot-andmouth disease virus replication. Virus Res
(1968). Foot-and-mouth disease. Annu Rev Microbiol
(1999). JJS: Origin and evolution of viruses.
(1995). King AM: Viral RNA modulates the acid sensitivity of foot-and-mouth disease virus capsids.
(2007). Mateu MG: Deterministic, compensatory mutational events in the capsid of foot-and-mouth disease virus in response to the introduction of mutations found in viruses from persistent infections.
(2009). Meneses PI: The role of NH4Cl and cysteine proteases in Human Papillomavirus type 16 infection. Virol J
(2003). Molecular basis of pathogenesis of FMDV. Virus Res
(2006). Mouse polyomavirus enters early endosomes, requires their acidic pH for productive infection, and meets transferrin cargo in Rab11-positive endosomes.
(2004). Novella IS: Vesicular stomatitis virus evolution during alternation between persistent infection in insect cells and acute infection in mammalian cells in dominated by the persistence phase.
(1959). Observations on the carrier state of cattle exposed to foot and mouth disease virus. Tijdschr Diergeneeskd
(1957). RE: A plaque assay for foot-andmouth disease virus and kinetics of virus reproduction. Virology
(1985). RH: Early steps in FMDV replication: further analysis on the effects of chloroquine. Virology
(1984). RH: Effect of lysosomotropic agents on the foot-and-mouth disease virus replication. Virology
(2010). Sobrino F: A single amino acid substitution in the capsid of foot-and-mouth disease virus can increase acid lability and confer resistance to acid-dependent uncoating inhibition.
(2009). T: A dominantnegative mutant of rab5 inhibits infection of cells by foot-and-mouth disease virus: implications for virus entry.
(1997). TS: Reovirus variants selected during persistent infections of L cells contain mutations in the viral S1 and S4 genes and are altered in viral disassembly.