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Persistent infection of C3H/St mice with certain strains of lymphocytic choriomeningitis virus (LCMV) causes a growth hormone (GH) deficiency syndrome (GHDS) manifested as growth retardation and hypoglycemia. Infected mice show high levels of viral replication in the GH-producing cells in the anterior pituitary leading to decreased synthesis of GH mRNA and protein despite the absence of detectable virus-induced cell structural damage. Virus clones isolated from the GHDS-negative LCMV WE strain can cause the disease, while others cannot. The genetic basis of this phenotypic difference is a nucleotide substitution resulting in a single amino acid difference in the viral glycoprotein. Reassortant studies indicate that the single amino acid substitution (Ser-153 to Phe) is sufficient to allow infection of the GH-producing cells and cause GHDS. These results show that a single change in the genome can affect viral pathogenicity by altering the tropism of the virus.

Original publication

DOI

10.1128/jvi.70.12.8438-8443.1996

Type

Journal article

Journal

Journal of virology

Publication Date

12/1996

Volume

70

Pages

8438 - 8443

Addresses

Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, USA.

Keywords

Cell Line, Animals, Mice, Inbred C3H, Mice, Reassortant Viruses, Lymphocytic choriomeningitis virus, Hypoglycemia, Syndrome, Growth Disorders, Glycoproteins, Phenylalanine, Serine, Viral Proteins, Cricetinae, Genetic Variation