Evolution and persistence mechanisms of mouse hepatitis virus.

[1]  M. Lai,et al.  Requirement of the 5'-end genomic sequence as an upstream cis-acting element for coronavirus subgenomic mRNA transcription , 1994, Journal of virology.

[2]  M. Lai,et al.  Coronavirus leader RNA regulates and initiates subgenomic mRNA transcription both in trans and in cis , 1994, Journal of virology.

[3]  R. Ley,et al.  The 5'-untranslated regions of picornavirus RNAs contain independent functional domains essential for RNA replication and translation , 1994, Journal of virology.

[4]  S. Weiss,et al.  MHV-A59 fusion mutants are attenuated and display altered hepatotropism. , 1994, Virology.

[5]  Stephen S. Morse,et al.  The Evolutionary biology of viruses , 1994 .

[6]  D. Brian,et al.  A translation-attenuating intraleader open reading frame is selected on coronavirus mRNAs during persistent infection. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[7]  M. Lai,et al.  Three different cellular proteins bind to complementary sites on the 5'-end-positive and 3'-end-negative strands of mouse hepatitis virus RNA , 1993, Journal of virology.

[8]  D. Brian,et al.  Leader-mRNA Junction Sequences Are Unique for Each Subgenomic mRNA Species in the Bovine Coronavirus and Remain So Throughout Persistent Infection , 1993, Virology.

[9]  E. Domingo,et al.  A single nucleotide substitution in the internal ribosome entry site of foot-and-mouth disease virus leads to enhanced cap-independent translation in vivo , 1993, Journal of virology.

[10]  J. Aiken,et al.  Persistence of viral RNA in the central nervous system of mice inoculated with MHV-4. , 1993, Advances in experimental medicine and biology.

[11]  K. Soike,et al.  Coronavirus infects and causes demyelination in primate central nervous system , 1992, Virology.

[12]  G. Scheper,et al.  The 5' untranslated region of encephalomyocarditis virus contains a sequence for very efficient binding of eukaryotic initiation factor eIF-2/2B. , 1991, Biochimica et biophysica acta.

[13]  K. Yamaguchi,et al.  Induction of self-reactive T cells after murine coronavirus infection , 1991, Journal of virology.

[14]  D. Brian,et al.  Bovine coronavirus mRNA replication continues throughout persistent infection in cell culture , 1990, Journal of virology.

[15]  R. Baric,et al.  Genetics of mouse hepatitis virus transcription: Identification of cistrons which may function in positive and negative strand RNA synthesis , 1990, Virology.

[16]  J. Fleming,et al.  Monoclonal antibodies to the peplomer glycoprotein of coronavirus mouse hepatitis virus identify two subunits and detect a conformational change in the subunit released under mild alkaline conditions , 1990, Journal of virology.

[17]  S. Perlman,et al.  Identification of the spinal cord as a major site of persistence during during chronic infection with a murine coronavirus , 1990, Virology.

[18]  S. Sawicki,et al.  Coronavirus transcription: subgenomic mouse hepatitis virus replicative intermediates function in RNA synthesis , 1990, Journal of virology.

[19]  M. Lai,et al.  High-frequency leader sequence switching during coronavirus defective interfering RNA replication , 1989, Journal of virology.

[20]  O. Elroy-Stein,et al.  Cap-independent translation of mRNA conferred by encephalomyocarditis virus 5' sequence improves the performance of the vaccinia virus/bacteriophage T7 hybrid expression system. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[21]  L. Weiner,et al.  Pathogenicity of antigenic variants of murine coronavirus JHM selected with monoclonal antibodies , 1986, Journal of virology.

[22]  V. ter meulen,et al.  Adaptation of coronavirus JHM to persistent infection of murine sac(-) cells. , 1984, The Journal of general virology.

[23]  L. Weiner,et al.  Antigenic relationships of murine coronaviruses: Analysis using monoclonal antibodies to JHM (MHV-4) virus , 1983, Virology.

[24]  S. Cheley,et al.  Fusion resistance and decreased infectability as major host cell determinants of coronavirus persistence , 1983, Virology.

[25]  R. Knobler,et al.  Virus persistence and recurring demyelination produced by a temperature-sensitive mutant of MHV-4 , 1982, Nature.

[26]  K. Holmes,et al.  Evolution of a coronavirus during persistent infection in vitro. , 1981, Advances in experimental medicine and biology.

[27]  S. Makino,et al.  Persistent infection with mouse hepatitis virus, JHM strain in DBT cell culture. , 1981, Advances in experimental medicine and biology.

[28]  V. Meulen,et al.  Biochemistry and Biology of Coronaviruses , 1981, Advances in Experimental Medicine and Biology.

[29]  L. Weiner,et al.  Characterization of the cold-sensitive murine hepatitis virus mutants rescued from latently infected cells by cell fusion , 1979, Virology.

[30]  L. Weiner,et al.  Rescue of a positive stranded RNA virus from antigen negative neuroblastoma cells. , 1979, Life sciences.

[31]  W. Flintoff,et al.  In vivo and in vitro models of demyelinating diseases II. Persistence and host-regulated thermosensitivity in cells of neural derivation infected with mouse hepatitis and measles viruses , 1978, Virology.