Penetration and uncoating of frog virus 3 (FV3) in cultured rat Kupffer cells
References (30)
- et al.
Vaccinia as a model for membrane biogenesis
Virology
(1968) Entry of an insect Poxvirus by fusion of the virus envelope with the host cell membrane
Virology
(1973)- et al.
Electron microscopic observations on early events of Frog Virus 3 replication
Virology
(1974) Early interactions of viruses with cellular membranes
Advan. Virus Res.
(1979)The structure of icosahedral cytoplasmic deoxyriboviruses. II. An alternative model
J. Ultrastruct. Res.
(1973)- et al.
Lipid composition of Frog virus 3
Virology
(1974) Observations on the fine structure and peroxidase cytochemistry of normal Rat liver Kupffer cells
J. Ultrastruct. Res.
(1974)- et al.
The mode of entry of Vaccinia Virus into L cells
J. Gen. Virol.
(1973) - et al.
The effect of FV3 structural proteins on cellular protein synthesis
- et al.
Preparation and properties of an inhibitory extract from Frog Virus 3 particles
J. Virol.
(1973)
Etude morphologique séquentielle du développment du FV3 sur cellules BHK21
J. Microsc.
Early events in cell-animal virus interaction
Bacteriol. Rev.
Penetration of animal viruses into cells
Viropexis, the mechanism of Influenza virus infection
Nature (London)
Interaction of Frog Virus 3 (FV3) with sinusoidal cells
Cited by (31)
Largemouth bass ranavirus: Current status and research progression
2023, Aquaculture ReportsPrior induction of cellular antiviral pathways limits frog virus 3 replication in two permissive Xenopus laevis skin epithelial-like cell lines
2021, Developmental and Comparative ImmunologyCitation Excerpt :Our findings support the use of Xela DS2 and Xela VS2 to replicate FV3 and for use as in vitro models in which interactions between frog skin epithelial cells and FV3 can be examined. FV3 exists as enveloped and non-enveloped/naked virions and is known to enter host cells through receptor-mediated endocytosis (enveloped virions) or fusion at the plasma membrane followed by nucleocapsid injection into the cytoplasm (naked virions) (Braunwald et al., 1985; Gendrault et al., 1981; Houts et al., 1974; Kelly, 1975). In contrast to previous studies that suggest FV3 uses class A scavenger receptors for cellular entry in tadpole cell lines (American toad, wood frog, green frog, bullfrog) and adult X. laevis macrophages (Vo et al., 2019a), Xela DS2 and Xela VS2 do not express appreciable levels of class A scavenger receptor (srai/ii, scara3, scara4, scara5, and marco) transcripts despite being susceptible and permissive to FV3.
Ranaviruses and other members of the family Iridoviridae: Their place in the virosphere
2017, VirologyCitation Excerpt :Although an envelope is not needed to initiate a productive viral infection, the presence or absence of an envelope appears to determine the route of entry and the specific infectivity of the virion. Early studies indicated that enveloped viruses enter by receptor-mediated endocytosis whereas non-enveloped virions initiate infection by binding the plasma membrane with subsequent entry of the viral core into the cytoplasm (Braunwald et al., 1985, 1979; Gendrault et al., 1981; Liu et al., 2016). Recently entry via pinocytosis or caveolin-mediated mechanisms have been proposed (Guo et al., 2011, 2012; Jia et al., 2013; Wang et al., 2014).
Delineating the roles of cellular and innate antiviral immune parameters mediating ranavirus susceptibility using rainbow trout cell lines
2017, Virus ResearchCitation Excerpt :FV3 preparations contain both enveloped particles and non-enveloped (naked) particles (Chinchar et al., 2011). While receptor-mediated endocytosis is one of two possible modes of entry, the other being fusion, it is likely the primary route (Gendrault et al., 1981; Braunwald et al., 1985; Chinchar, 2002). Thus, RTG-2 may express more surface receptors, to date of unknown identity, or have higher endocytic activity, to enhance virus attachment and entry respectively.
Amphibian (Xenopus laevis) tadpoles and adult frogs mount distinct interferon responses to the Frog Virus 3 ranavirus
2017, VirologyCitation Excerpt :Interestingly, murine FV3 infection models were employed for hepatitis research over 30 years ago (Gut et al., 1981; Kirn et al., 1982, 1980). While the temperature of 37 °C used for these studies are not permissive to FV3 replication (Aubertin et al., 1973), these studies demonstrated viral cell entry and release of viral content into host cell cytoplasm (Gendrault et al., 1981). In absence of viral replication, the FV3-induced pathology observed in these early studies would have had to stem from pre-packaged factors already present in the FV3 virions.