SUB TRACK: Coronavirus Pathogenesis, SARS-CoV, pathogenesis, Epidemiology, pathogenesis, diagnosis and treatment of COVID-19, infectious disease, prevention,
Many species, including humans, are infected by coronaviruses, which can cause both acute and chronic illnesses. The pathophysiology of murine coronaviruses, including mouse hepatitis virus (MHV) and severe acute respiratory coronavirus, is the main emphasis of this paper (SARS-CoV). One of the few animal models for the study of persistent demyelinating illnesses like multiple sclerosis, MHV is a collection of strains that offer models systems for the research of viral tropism and pathogenesis in numerous organ systems, including the central nervous system, the liver, and the lung. SARS-CoV first infected humans in China in 2002, sparking a pandemic with severe morbidity and significant fatality rates, especially in the elderly. We review the viral and bacterial pathogenesis,
The family of viruses known as coronaviruses includes a number of viruses that can infect both people and animals. Some human coronaviruses produce more serious sickness, whereas others just cause mild illness like the common cold (such as MERS – Middle East Respiratory Syndrome and SARS – Severe Acute Respiratory Syndrome). In December 2019, a new coronavirus that has not before been discovered in humans appeared in Wuhan, China.
Respiratory symptoms such as fever, coughing, and shortness of breath are signs and symptoms. When an infection is more severe, it may result in pneumonia, severe acute respiratory syndrome, and even fatalities. Regular hand washing with soap and water or an alcohol-based hand rub is advised to stop the spread of COVID-19, as is elbow flexion to cover the nose and mouth.
A. Pathogenesis of MHV
A variety of strains with various organ tropisms make up the MHV. Based on common tropism patterns, the two primary biotypes of MHV strains can be distinguished. The MHV-D, -Y, -RI, -S/CDC, LIVIM, and DVIM are among a group of enterotropic viruses that frequently produce MHV epidemics in confined mouse colonies (Homberger et al., 1998). The other biotype, the polytropic strains, are typically investigated as illness models in humans. This group’s many strains serve as model systems for a number of organ system illnesses. Chronic demyelinating disorders and acute encephalitis are caused by neurotropic MHV strains.
- illness of the central nervous system
The neurotropic MHV strains, particularly JHM and A59, are the ones that are investigated the most. The first JHM isolate was found in a paralysed mouse and was extremely neurovirulent, causing severe demyelination and encephalomyelitis (Bailey et al., 1949, Cheever et al., 1949). After that, it was repeated twice via mouse brains (Lavi et al., 1984a, Weiner, 1973, Weiner et al., 1973). There is some misunderstanding over the true phenotype of JHM because multiple clones with very diverse pathogenic characteristics were obtained and used in many labs from this mouse brain-adapted strain. In recent years, efforts have been made to distinguish between the JHM isolates,
MHV-induced hepatitis has been researched using a variety of strains, including the more modestly hepatotropic A59 and the extremely hepatovirulent MHV-3 and MHV-2. The VS weanling mouse that had acute hepatitis after being injected with serum from a person who had acute hepatitis led to the isolation of the MHV-3 strain, which is most frequently used to research the pathogenesis of MHV-induced hepatitis (Dick et al., 1956). When administered to naive mice, a liver homogenate from this initial isolation did not cause any clinical symptoms. However, similar to the neurovirulence of JHM, a virus that caused fulminant hepatitis and was fatal for weanling VS mice appeared after serial passage of MHV3 in suckling or weanling mice. This virus, known as MHV-3, was largely hepatotropic and caused severe liver necrosis (Dick et al., 1956).
Age and mice strain affect the amount of the liver damage brought on by MHV-3 (Le Prevost et al., 1975). The majority of strains, including DBA/2, BALB/c, and C57BL/6, are extremely prone to fatal illness. A/J mice are extremely resistant, while C3H mice are only somewhat sensitive (Le Prevost et al., 1975). After infection of susceptible mice, pathology, which is characterised by necrotic foci and inflammatory infiltrates of neutrophils and mononuclear cells, develops swiftly and peaks 3–4 days later, coinciding with the peak of viral replication (Dick et al., 1956).
Unlike the strains previously mentioned, the MHV-1 virus is predominantly pneumovirulent. The A/J mouse strain, which is resistant to MHV-3-induced hepatitis, is the most sensitive to MHV-1-induced pneumonitis. While MHV-1 infection of A/J mice provides a murine model for the pathogenesis of SARS-CoV in humans, Balb/c and C57Bl/6 mice are resistant to MHV-1-induced lung illness (De Albuquerque et al., 2006). A/J mice infected with MHV-1 intranasally develop consolidated pneumonitis, which is marked by hyaline membranes, fibrin deposition, lymphocytic infiltration, and macrophage infiltration, and they pass away 7 days after infection. The majority of viral particles are detected in pulmonary macrophages. The resistance/susceptibility pattern in C3H/HeJ mice is intermediate; they develop chronic lung fibrosis and bronchial hyperplasia, and 40% of the mice pass away by day 28. All mouse strains replicated the MHV-1 virus.