Mousepox Virus (PVM)

In a 1939–1940 study, researchers attempted to isolate a certain human virus by repeatedly passing nasal and pharyngeal washes from patients with respiratory infections through mice. They found that both inoculated and non-inoculated mice often developed pulmonary consolidation in their lungs. Subsequently, a pneumotropic virus—known as Mouse Pneumonia Virus (PVM)—was isolated from the lungs of normally healthy mice. Notably, this virus lost its virulence after being passaged only a few times, yet the study also demonstrated that latent infections with this virus are widespread within mouse populations.

PVM belongs to the Paramyxoviridae family and the Pneumovirus genus, which also includes certain respiratory syncytial viruses found in humans and cattle. While PVM exhibits distinctly different antigenic properties compared to all other members of the Paramyxoviridae family, it shares several other characteristics with both respiratory syncytial virus and measles virus. Notably, strains of PVM isolated from either mice or hamsters show identical properties, suggesting that all PVM strains likely share the same antigenicity. Furthermore, when the virus is continuously passaged through mouse lungs, the resulting viral strain isolated from mouse lungs becomes more virulent—implying that differences in virulence among various PVM strains may indeed exist. Interestingly, PVM grown in baby hamster kidney (BHK-21) cells displays antigenic properties similar to those of the virus propagated in mouse lungs, though it tends to be slightly less virulent in mice.

PVM is a strictly lung-tropic virus whose particles exhibit pleomorphism, typically appearing as 100-nm-diameter, 3-µm-long filaments, though occasionally they can also be spherical, measuring 80–200 nm in diameter. The virus contains a helical, single-stranded RNA genome. Notably, it can replicate efficiently within the lungs for an extended period, with a replication cycle that occurs in a discontinuous manner—on average, viral titers increase by 7.9-fold per day, though this rapid rise begins to plateau only after approximately the 16th day post-infection. Following intranasal inoculation, the majority (90%) of the administered virus is cleared from the respiratory tract. A latent period of about 15 hours ensues after inoculation, during which the virus accumulates in the lungs at a rate exceeding the total multiplication observed over the subsequent 10–15 hours of the full 24–30-hour replication cycle. During each replication cycle, the virus undergoes nearly 16-fold amplification, and the peak viral titers in mouse lung tissue can reach nearly 10^2.5 LD50/ml or even 10^5.5 LD50/ml. Importantly, the time required to achieve peak viral titers in the lungs is directly proportional to the dose of the virus administered; however, the maximum titer itself remains unaffected by the infection dose. Typically, peak viral titers are observed between 6 and 8 days post-infection, after which they begin to decline steadily by the ninth day. By two weeks post-infection, the virus is no longer detectable. The virus can efficiently replicate in primary hamster kidney cells (HKKC), BHK-21, Vero cells, and hamster embryo cells. Notably, cytopathic effects (CPE) induced in Vero cells develop gradually and remain incomplete even by the 11th day, without forming syncytia. At 24 hours post-infection, inclusion bodies become visible within the cytoplasm. Furthermore, viral antigens accumulated inside infected cells can be detected via immunofluorescence assay (IFA) as early as 16 to 24 hours post-infection.

PVM is primarily transmitted via direct contact and airborne aerosol transmission. Naturally infected hosts are limited to laboratory rodents: mice, hamsters, rats, jerboas, and guinea pigs. Younger rodents are more susceptible than older ones, but a more critical factor influencing susceptibility appears to be diet. (The impact of sex on infection differences remains uncertain.)

PVM is typically diagnosed using serological methods (ELISA, IFA, MFIA), and PCR can also be employed (on lung tissue and tracheal samples). Importantly, all PVM strains share the same antigenic properties.

Wild rodents may serve as reservoir hosts for PVM, so it’s crucial to prevent wild rodents from entering facilities. Routine serological testing of the colony population is recommended, along with quarantine and isolation of any suspicious animals introduced into the facility. For infected animals, the appropriate course of action depends on their value and the availability of suitable replacements. Generally, complete culling is advised, followed by thorough disinfection of animal housing areas and reintroduction of new, healthy animals. Uterine extirpation combined with embryo transplantation has been proven effective in eradicating Mouse Pneumonia Virus. In immunocompetent animals, temporarily halting breeding until the infection is cleared can also be a successful strategy. However, such measures should only be attempted under close monitoring and stringent control. Additionally, using cages equipped with filter lids, minimizing human activity, and implementing rigorous husbandry practices can help limit the spread of PVM.

References

1. "Journal of Laboratory Animal Science" 2(2) 45-51; 1985; John G. Parker; Conrad B. Richter

2. DISEASES OF RESEARCH ANIMALS - DORA; University of Missouri - Comparative Medicine Program and IDEXX-RADIL

3. Common Pathogen Information from Tsinghua University's Laboratory Animal Center

4. 4. Division of Animal Resources, University of Illinois, Urbana