Journal of General Virology
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Identification of human papillomavirus seroconversions
Journal of General Virology - Tập 76 Số 3 - Trang 529-539 - 1995
Assembled baculovirus-expressed human papillomavirus type 11 L1 capsid protein virus-like particles are recognized by neutralizing monoclonal antibodies and induce high titres of neutralizing antibodies
Journal of General Virology - Tập 75 Số 9 - Trang 2271-2276 - 1994
Human papillomavirus (HPV) type 11 recombinant virus-like particles induce the formation of neutralizing antibodies and detect HPV-specific antibodies in human sera
Journal of General Virology - Tập 75 Số 8 - Trang 2075-2079 - 1994
Prophylactic and therapeutic vaccination against a mucosal papillomavirus
Journal of General Virology - Tập 74 Số 6 - Trang 945-953 - 1993
Biological Markers for Differentiation of Herpes-virus Strains of Oral and Genital Origin
Journal of General Virology - Tập 4 Số 2 - Trang 259-267 - 1969
The Complete Nucleotide Sequence of Potato Virus X and Its Homologies at the Amino Acid Level with Various Plus-stranded RNA Viruses
Journal of General Virology - Tập 69 Số 8 - Trang 1789-1798 - 1988
Formation of Non-infective Herpesvirus Particles in Cultured Cells Treated with Human Interferon
Journal of General Virology - Tập 65 Số 6 - Trang 1069-1078 - 1984
Diverse host–virus interactions following caprine arthritis-encephalitis virus infection in sheep and goats Interspecies transmissions substantially contribute to the epidemiology of small ruminant lentiviruses (SRLVs), including caprine arthritis encephalitis virus (CAEV) and visna-maëdi virus. However, comprehensive studies of host–virus interactions during SRLV adaptation to the new host are lacking. In this study, virological and serological features were analysed over a 6 month period in five sheep and three goats experimentally infected with a CAEV strain. Provirus load at the early stage of infection was significantly higher in sheep than in goats. A broad antibody reactivity against the matrix and capsid proteins was detected in goats, whereas the response to these antigens was mostly type-specific in sheep. The humoral response to the major immunodominant domain of the surface unit glycoprotein was type-specific, regardless of the host species. These species-specific immune responses were then confirmed in naturally infected sheep and goats using sera from mixed flocks in which interspecies transmissions were reported. Taken together, these results provide evidence that SRLV infections evolve in a host-dependent manner, with distinct host–virus interactions in sheep and goats, and highlight the need to consider both SRLV genotypes in diagnosis, particularly in sheep.
Journal of General Virology - Tập 94 Số 3 - Trang 634-642 - 2013
Mutations in the G–H loop region of ephrin-B2 can enhance Nipah virus binding and infection Nipah virus (NiV) and Hendra virus (HeV) are zoonotic paramyxoviruses classified in the genus Henipavirus of the family Paramyxoviridae . The entry of henipaviruses occurs through a pH-independent membrane-fusion mechanism mediated by the cooperation of the viral attachment (G) and fusion (F) envelope glycoproteins following virion binding to susceptible host cells. Virus attachment is mediated by the interaction of the G glycoprotein with ephrin-B2 or ephrin-B3, which were identified as the functional receptors of henipavirus. Several residues of the G glycoprotein that are important for receptor binding have been determined through mutagenesis and structural analyses; however, similar approaches have not been carried out for the viral receptor ephrin-B2. Here, an alanine-scanning mutagenesis analysis was performed to identify residues of ephrin-B2 which are critical for NiV binding and entry by using an NiV-F- and -G-glycoprotein pseudotyped lentivirus assay. Results indicated that the G–H loop of ephrin-B2 was indeed critical for the interaction between ephrin-B2 and NiV-G. Unexpectedly, however, some alanine-substitution mutants located in the G–H loop enhanced the infectivity of the NiV pseudotypes, in particular an L124A mutation enhanced entry >30-fold. Further analysis of the L124A ephrin-B2 mutant demonstrated that an increased binding affinity of the mutant receptor with NiV-G was responsible for the enhanced infectivity of both pseudovirus and infectious virus. In addition, cell lines that were stably expressing the L124A mutant receptor were able to support NiV infection more efficiently than the wild-type molecule, potentially providing a new target-cell platform for viral isolation or virus-entry inhibitor screening and discovery.
Journal of General Virology - Tập 92 Số 9 - Trang 2142-2152 - 2011
T7 RNA polymerase-dependent and -independent systems for cDNA-based rescue of Rift Valley fever virus Rift Valley fever virus (RVFV) is responsible for large and recurrent outbreaks of acute febrile illness among humans and domesticated animals in Africa. It belongs to the family Bunyaviridae , genus Phlebovirus , and its negative-stranded RNA genome consists of three segments. Here, we report the establishment and characterization of two different systems to rescue the RVFV wild-type strain ZH548. The first system is based on the BHK-21 cell clone BSR-T7/5, which stably expresses T7 RNA polymerase (T7 pol). Rescue of wild-type RVFV was achieved with three T7 pol-driven cDNA plasmids representing the viral RNA segments in the antigenomic sense. The second system involves 293T cells transfected with three RNA pol I-driven plasmids for the viral segments and two RNA pol II-driven support plasmids to express the viral polymerase components L and N. It is known that the 5′ triphosphate group of T7 pol transcripts strongly activates the antiviral interferon system via the intracellular RNA receptor RIG-I. Nonetheless, both the T7 pol and the pol I/II system were of similar efficiency. This was even true for the rescue of a RVFV mutant lacking the interferon antagonist nonstructural proteins. Further experiments demonstrated that the unresponsiveness of BHK-21 and BSR-T7/5 cells to T7 pol transcripts is most probably due to a deficiency in the RIG-I pathway. Our reverse genetics systems now enable us to manipulate the genome of RVFV and study its virulence mechanisms. Moreover, the finding that BHK-derived cell lines have a compromised RIG-I pathway may explain their suitability for propagating and rescuing a wide variety of viruses.
Journal of General Virology - Tập 89 Số 9 - Trang 2157-2166 - 2008
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