Differential Susceptibility of Male and Female Mice to Encephalomyocarditis Virus: Effects of Castration, Adrenalectomy, and the Administration of Sex Hormones

Friedman, Stanford B.; Grota, Lee J.; Glasgow, Lowell A.

doi:10.1128/iai.5.5.637-644.1972

Cited by 45 publications

(19 citation statements)

References 27 publications

(27 reference statements)

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“…Estrone stimulates the replication of both viruses and appears to make previously resistant tissues susceptible to MM virus. DISCUSSION Previous studies indicate that certain steroids enhance experimental viral infections, whereas others have little or no effect (1,2,4,8,10,11). The present study, however, has shown that the VIE activity of a hormone may be dependent on the viral agent used for challenge.…”

Section: Resultscontrasting

confidence: 62%

Further Studies on the Influence of Steroids on Viral Infection in Mice

et al. 1973

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Certain steroids have been reported to enhance experimental viral infections, whereas others have little or no effect. Interference with the interferon system has been suggested as a possible mechanism for the viral infection-enhancing (VIE) activity of hormones. In the present study, steroids (prednisolone, progesterone, testosterone) which had no effect on MM virus infection demonstrated VIE activity against Mayaro virus infection. It is suggested that the VIE activity of a hormone may be dependent on the viral agent used for challenge. Data are also presented which suggest that, in addition to interference with the interferon system, the VIE activity of steroid hormones may be the result of at least two other actions: (i) alteration of cell membranes; (ii) stimulation of initial viral replication.

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Section: Resultscontrasting

confidence: 62%

Further Studies on the Influence of Steroids on Viral Infection in Mice

et al. 1973

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“…Also, female backcross progeny consistently were more resistant than their male counterparts. Enhanced resistance to various viral and bacterial pathogens of female as compared with male mice has been well documented (17)(18)(19)(20)(21)(22). It also has been shown in immunized outbred Swiss mice challenged i.c.…”

Section: Discussionmentioning

confidence: 95%

Genetic control of resistance to street rabies virus in mice.

Lodmell¹

1983

The Journal of Experimental Medicine

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Resistance to intraperitoneally inoculated street rabies virus (SRV) in mice was shown to be under genetic control. SJL/J, CBA/J, DBA/2J, and BALB/cAn mice were resistant, whereas A/WySn/J and A.SW/SnJ mice were susceptible. In addition, female mice of the resistant BALB/cAn and DBA/2J strains were more resistant than their male counterparts. Resistance was not controlled solely by the major histocompatibility locus because susceptible A.SW/SnJ and resistant SJL/J mice have the same H-2S haplotype. Challenge of F1 hybrids produced by crossing resistant and susceptible strains indicated resistance was dominant (97% survivors). Inoculation of backcross mice produced by mating F1 hybrids with susceptible parents showed that one and/or two genes controlled susceptibility. Furthermore, inoculation of SRV obtained from six different animals indicated that differences in strain susceptibilities were not dependent on the SRV isolate. Genetic control of resistance to SRV was, however, abrogated by intracerebral inoculation of virus. Resistant strains of mice were detected that either remained asymptomatic or, in contrast, developed signs of clinical disease, but disease failed to progress and they survived. The recognition of resistant and susceptible strains of mice, differences in female-male resistance within the same resistant strain, as well as dissimilar clinical responses in different resistant mouse strains to intraperitoneally inoculated SRV provide promising probes for investigation of host resistance and mechanisms for survival after onset of clinical rabies.

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“…Alternately, hormonal differences may make the pancreas in the male more susceptible to virus-induced injury. In this connection, it is known that EMC virus produces more severe disease and higher mortality in males than females (16). The observation that hyperglycemia persists in the males for many months after infectious virus can be recovered from the pancreas suggests that the infection produces acute beta cell damage that in some cases results in permanent impairment of function.…”

Section: Discussionmentioning

confidence: 99%

Virus-Induced Diabetes Mellitus

Boucher

Notkins

1973

The Journal of Experimental Medicine

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Infection of DBA/2N male mice with encephalomyocarditis virus resulted in a diabeteslike syndrome characterized by hyperglycemia, glycosuria, hypoinsulinemia, polydipsia, and polyphagia. Blood glucose levels were elevated within 4 days after infection and reached a maximum mean level of 320 mg/100 ml within 12 days. Approximately 60–80% of the animals developed a transient hyperglycemia while 10–15% of the animals remained hyperglycemic for well over 6 mo. The remaining animals failed to become hyperglycemic but many had abnormal glucose tolerance curves. Hyperglycemia was most pronounced when animals were allowed free access to food, and the incidence of byperglycemia was related both to the strain and sex of the animals, with few females developing hyperglycemia. The amount of immunoreactive insulin in the plasma of infected hyperglycemic mice was significantly lower than in appropriate controls, and injection of exogenous insulin resulted in a rapid drop in the blood glucose levels. Despite the fact that certain animals were hyperglycemic for many months, virus could not be recovered from the pancreas after the first 10 days of the infection.

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Differential Susceptibility of Male and Female Mice to Encephalomyocarditis Virus: Effects of Castration, Adrenalectomy, and the Administration of Sex Hormones

Cited by 45 publications

References 27 publications

Further Studies on the Influence of Steroids on Viral Infection in Mice

Further Studies on the Influence of Steroids on Viral Infection in Mice

Genetic control of resistance to street rabies virus in mice.

Virus-Induced Diabetes Mellitus

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