In Vitro Interaction of Mouse Hepatitis Virus and Macrophages From Genetically Resistant Mice

Abstract

Peritoneal macrophages from genetically resistant C3H mice and genetically susceptible Princeton (PRI) mice adsorbed the MHV (PRI) strain of mouse hepatitis virus equally well. The difference between the permissive cells and the nonpermissive ones seems to reside in the ability of the former to "eclipse" the virus and, subsequently, support virus replication. C3H cells exposed to low multiplicities of the virus remained intact with no demonstrable viral replication. Virus, taken up by the resistant cells, was protected from heat and underwent slow inactivation while few or no virus particles were released into the medium.

Resistance of C3H/HeJ Mice to Lethal Challenge with Herpes Simplex Virus

“…Host susceptibility to viral infections is obviously determined by a complex series of factors (10). In a recent study, Lopez suggested that resistance to HSV-1 in mice was determined by at least three genes (1 1).…”

A Major Role of Macrophage Activation by Interferon-Gamma during Mouse Hepatitis Virus Type 3 Infection. I. Genetically Dependent Resistance

“…We have recently described that a nutritionally induced impairment of the Kupffer cell functions, such as the sensitivity to IFN, was pertinent to the loss of resistance as shown by hypercholesterolemic AI] mice during the MHV3 infection (6). The genetically determined capacity of macrophages to restrict MHV3 multiplication has been considered to be one of the most important factors in determining in vivo susceptibility or resistance (1,4,7). However, the treatment of resistant mice with anti-lymphocytic sera or Xirradiation induces susceptibility (8), indicating that Met> alone probably do not account for all instances of resistance.…”

The Biology of Coronaviruses

“…Infections can also be modulated by lymphokines and interferons secreted from T lymphocytes and by corticosteroid hormones. Also macrophages secrete interferon, complement, chemotactic substances and prostaglandins, all of which influence viral replication, and these functions can be impaired or enhanced during chronic infections (Arnheiter et al, 1982;Bang & Warwick, 1960;Dupuy et al, 1975;Knobler et al, 1981 b;Krzystyniak & Dupuy, 1981 ;Lahmy & Virelizier, 1981 ;Levy-Leblond & Dupuy, 1977;Levy-Leblond et al, 1979;Sheets et al, 1978;Shif & Bang, 1970;Stohlman & Frelinger, 1978;Stohlman et al, !980;Taguchi et al, 1976;Tardieu et al, 1980;Taylor et al, 1981 ;Virelizier & Gresser, 1978;.…”