key: cord-0004884-rjl35dpa authors: Taguchi, F.; Yamada, A.; Fujiwara, K. title: Asymptomatic infection of mouse hepatitis virus in the rat date: 1979 journal: Arch Virol DOI: 10.1007/bf01317424 sha: eca2198b86a6d3c0e91d9846d003c6db3b7f8780 doc_id: 4884 cord_uid: rjl35dpa After intranasal inoculation of suckling rats mouse hepatitis virus multiplied mostly in the nasal epithelium; though there were no symptoms, antibodies were produced. Antibodies were also demonstrated in adult rats. These findings suggest that the rat may be a natural host for the virus. , MHV-S multiplied in the "anterior part of the head", which includes the nasal bones as well as the nasal mucosa, and reached a maximum titer of about 10 5 PFU/0.2 g on day 2. Virus grew to much lower titres in the brain and low titres (less than 10 2 PFU/0.2 g) were also detected in the lung, liver and spleen in some animals examined 1 to 4 days after virus inoculation. Other tissues, such as salivary glands or blood, contained no infectious virus. limited to the nasal mueosa and brain (manuscript in preparation). Two other strains of MHV, namely JHM and MHV-Nu66 (10), were also inoculated into 10-day-old rats and were found to multiply, but to a lesser extent than MHV-S. Figs. 2a and 2b. Necrotic changes (Fig. 2a) and cytoplasmic immunofluorescenee (Fig. 2b) in epithelial cells of the nasal mueosa. Tissue from 10-day-old rats 2 days after i.n. inoculation with 105 PFU of MHV-S. Bar represents 0.1 mm Two-, 4-, 6-and t0-week-old rats were also inoculated i.n. with t05 PFU of MHV-S and infectious viruses were assayed in the lung, brain, salivary glands and liver. In less than one-third of the total, were infectious viruses detected in the lung and salivary glands and the titers were less than t02 PFU/0.2 g. No infectious virus was demonstrable in the liver. Sera were collected 14 days after inoculation and examined for neutralizing antibody. Table 1 shows that almost all contained neutralizing antibody to a titre of >100. The two rats inoculated at 6 weeks and seronegative when tested at 1 : 100 were nevertheless positive at i : 50. So far only mice have been considered to be natural hosts of MHV and rat; has been excluded because highly virulent MHV inoculated by various routes did not cause any sy~lptomatic infection like that produced in the mouse (7, 13) . However, this does not imply that MtIV does not infect the rat. In the present study, we clearly demonstrated that by the intranasal route MHV-S infects rats of various ages from the following criteria: 1. MHV replicated in the "anterior part of the head" and several other organs; 2. viral antigen was detected by immunoftuoreseenee in the epithelial cells of nasal mneosa where histopathological changes were also found ; 3. rats of all ages produced neutralizing antibodies after virus inoculation. I n some cases, neither infectious virus nor histopathologieal changes were demonstrable in infected rats, however, neutralizing antibodies were constantly detected in the sera of inoculated rats, revealing that MHV replication occurs in every cases, but m a y be below the detection level in some cases. Two eoronaviruses, namely rat eoronavirus (RCV) (12) and sialodaeryoadenitis virus (SDAV) (11) , are known to infect and cause disease in the rat. These viruses multiply first in the epithelial cells of the nasal cavity and thereafter, they manifest their organ tropism i.e., RCV goes to the respiratory system and woduees interstitial pneumonia (2, 12) and SDAV affects the salivary and lacrymal glands, and produces adenitis (11) . The pathogenesis of NHV-S infection in rats resembles, in part, that of SDAV or I~CV, in that these viruses cause the necrotic changes in the epithelial cells of the nasal mucosa at early stage of infection (2) . However MHV is confined there, or affects slightly the central nervous system as it does in infections of mice (manuscript in preparation). B~tATT and his eoworkers showed that SDAV multiplied in mice producing some histopathological changes in the respiratory system after i.n. inoculation (3) and we demonstrated in the w e s e n t paper that 3{HV infected rats of any ages. These facts indicate that SDAV and MItV are infectious for both mice and rats, so that both m a y play an important part in the survival of these viruses. A murine virus (JHM) causing disseminated encephalitis with extensive destruction of myelin. II Experimental infection of adult axenic rats with Parker's coronavirus Respiratory infection in mice with sialodacryoattenitis virus, a coronavirus of rats Lethal enteritis in infant mice caused by mouse hepatitis virus A rnurine virus (JHM) causing disseminated encephalitis with extensive destruction of myelin. I. Isolation and biological properties of the virus Problems in checking inapparent infections in laboratory mouse colonies. An attempt at serological checking by anamnestic response Mouse hepatitis virus and its pathogenic action Antibodies to mouse hepatitis virus in human sera Pathogenicity of mouse hepatitis virus for mice depending upon host age and route of infection Isolation of low-virulent mouse hepatitis virus from nude mice with wasting syndrome and hepatitis Pathogenesis of sialodaeryoadenitis in gnotobiotic rats Rat eoronavirus (1%CV): a prevalent, naturally occurring pneumotie virus of rats Experimental viral hepatitis Mouse hepatitis virus infection as a. highly contagious, prevMent, enteric infection of mice Difference in response to mouse hepatitis virus a, mong suseeptible mouse strMns Age-dependent response of mice to a mouse hepatitis virus, MttV-S. Japan We th~nk Dr. T. Sato (Chugai pharmaceutical Co., LTD) and Dr. H. ikeda of the same Institute for their many helpful discussions of the research.This work was supported partly by Grant-in-Aid for Scientific Research from Ministry of Education, Science and Culture, Japan.