F. Deinhardt

Morphology of the GB hepatitis agent.

ATTEMPTS to isolate hepatitis A virus have been in progress for several decades. An important advance was the finding that the marmoset served as a permissive animal host for this virus1, but it became obvious that more than one agent was active. The pedigree of one agent was established as MS-1 (hepatitis A) isolate, while the other, which was demonstrably different by neutralisation and cross-challenge experiments, was designated GB. The GB infectious serum was obtained on the third day of jaundice from a surgeon in Chicago who developed a mild form of acute hepatitis. This serum induced hepatitis in all four marmosets inoculated. A pool of infectious GB serum marmoset (passage 11) was prepared from the total bleeding of nine white-lipped marmosets (Saguinus sp.) 19–24 d after inoculation and during the early acute phase of hepatitis as indicated by an increase of serum transaminase levels. This pool, designated H 205 GB pass 11, has an infectivity of 104.5 marmoset ID50. We have now examined the GB agent electron microscopically, and found that it is smaller and more fragile than the MS-1 strain2, and therefore also the identical CR326 isolate3 of hepatitis A, which have the morphological appearances of recognised, small cubic viruses measuring about 27 nm in diameter.

Rubella and rheumatoid arthritis: hyaluronic acid and susceptibility of cultured rheumatoid synovial cells to viruses.

Summary Synovial cell lines were established from patients with rheumatoid arthritis (RA) and from normal human embryos. High levels of hyaluronic acid (HA) were produced by some RA cell lines, some of which were partially or completely resistant to infection with Newcastle disease virus (NDV), vesicular stomatitis virus (VSV), and rubella virus (RV). Normal fetal synovial cells lines were susceptible to NDV, VSV, and RV. Infection with virus became possible after treatment of RA cells with hyaluronidase to depolymerize HA, and HA prevented infection of normal synovial cells with VSV. These results provide evidence that HA and not chronic or latent viral infection is responsible for the lack of susceptibility of RA synovial cells to certain viruses.

Introduction to virus‐caused cancer: Type C virus

Ribonucleic acid‐containing, C‐type viruses have been isolated from almost every class of animals; they transform cells in vitro and cause leukemias and sarcomas in vivo. Although these viruses are structurally, biochemically, and biologically similar, they can be distinguished from each other by individually characteristic nucleic acids and antigens. They are usually transmitted vertically; evidence of their presence, in the form of nucleic acid sequences homologous to viral nucleic acid sequences, may be detected in normal cells. Many C‐type viruses are defective; helper viruses are needed for full viral genome expression. Human C‐type leukemia or sarcoma viruses have not been identified with certainty yet, although their existence can be predicted from the results of experimental animal studies and immunologic, ultrastructural, and biochemical analyses of human tumors.