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Persistent infection of cultivated cells with lymphocytic choriomeningitis virus: regulation of virus replication. Brief report.

L cells were infected with lymphocytic choriomeningitis virus (LCM virus). They were subcultivated and infectious virus and interfering virus were quantified at intervals. Both entities fluctuated in perfect parallelism. Superinfection with LCM virus revealed a pattern of interference that bore no simple relationship with the quantity of interfering virus present. We explain the oscillating pattern of virus replication, which characterizes this type of LCM virus carrier cultures, as being due to spontaneous shutdown of virus synthesis in conjunction with the action of a resistance factor produced by cells coinfected with infectious virus and interfering virus.

Animals↗

Equine infectious anemia virus (EIAV) humoral responses of recipient ponies and antigenic variation during persistent infection.

Three ponies were inoculated with plasma containing 10(4.8) TCID50 of equine infectious anemia virus (EIAV) and observed for 165 to 440 days. Each pony developed a febrile response within 3 weeks of infection during which a plasma viremia greater than or equal to 10(3.5) TCID50/ml was observed. Analyses of four isolates from sequential febrile episodes in a single pony were conducted by two-dimensional tryptic peptide maps and with monoclonal antibodies in immunoblots. Structural and antigenic alterations were observed in the envelope glycoproteins gp90 and gp45, with greatest variation in gp90. Specific IgG to EIAV gp90, gp45, and p26 of homologous and heterologous isolates was detectable by immunoblots within one month after infection although IgG levels to gp45 at this time were relatively low. The group-specific determinants of gp90 and gp45 were more antigenic than those of p26; however, binding of IgG to these determinants did not correlate with neutralization of EIAV as assayed in fetal equine kidney cells. Neutralizing antibodies were first detectable within two months of infection and only neutralized viruses isolated prior to serum collection. Neutralizing activity of sera collected later in the infection was broadly reactive regardless of the number of clinical episodes the donor had suffered.

Animals↗

Studies on a measles virus variant inducing persistent infections in cultured cells.I. Isolation and characterization of plaque purified virus clones.

Attempts were made to characterized by a plaque assay two variants of the Edmonston strain of measles virus and to obtain plaque purified virus populations. The UP non-cytocidal variant, in all the examined cell systems, mainly produced small but also large plaques; the DP cytocidal variant always large plaques. Three clones, UP-SP4, UP-LP4 and DP-LP4, were derived by plaque purfication respectively of the UP small plaque, UP large plaque and DP large plaque forming particles. The virus populations of the clones could be distinguished by some other biological and physical characters: cytopathic effect in roller tube cultures, growth potential in HeLa cells, thermal stability at 45 degrees C, stability of the properties during serial passages at different input multiplicity. The hypothesis was supported that the typical properties of the UP and DP variants are host-independent and genetically controlled viral markers.

Animals↗

Molecular evolution of HCV genotype 2c persistent infection following mother-to-infant transmission.

The molecular evolution of HCV 2c in a case of vertical transmission was studied by comparing the virus quasispecies in the sera from the mother and from the child in a two-year follow-up. The positivity of HCV-RNA since the delivery accounted for an in-utero infection. The Core-E1 genome region (nt 928-1225) was amplified by polymerase chain reaction (PCR) from serum samples collected at delivery and at 3, 9, 18 and 24 months after birth. The RIBA pattern was characterised by isolated anti-c22 positivity in the serum from mother and in sera from the child during the first 9 months. Additional presence of anti-c33 was observed afterwards. Genetic relatedness among isolates and with a mother minor variant serum (Mo1. 13) was found (mean variability ranged between 0.79% and 1.20%). From phylogenetic analysis this variant was identified as the origin of one of the two main lineages that included all isolates from child sera at 9, 18 and 24 months. The variability analysis has shown that high viral heterogeneity is present in the child serum collected at birth (3.16%). In this phase the dn/ds index (1.26%) indicates the presence of strong selective pressures. The development of child specific immune response at 9th month was concurrent with the disappearance of two mutants at positions 11 and 104 of E1. This rare case of in-utero mother-to-infant transmission can be considered as a model to elucidate the HCV quasispecies diversification during the first stage of infection.

Adult↗