ABSTRACT
Severe acute respiratory syndrome associated coronavirus 2 (SARS-CoV-2) emerged at the end of 2019 and rapidly caused a pandemic that led to the death of >6 million people due to hypercoagulation and cytokine storm. In addition, SARS-CoV-2 triggers a wide array of pathologies, including liver dysfunction and neurological disorders. It remains unclear if these events are due to direct infection of the respective tissues or result from systemic inflammation. Here, we explored the possible infection of hepatic and CNS cell lines by SARS-CoV-2. We show that even moderate expression levels of the angiotensin-converting enzyme 2 (ACE2) are sufficient for productive infection. SARS-CoV-2 infects hepatoma Huh7.5 and HepG2 cells but not non-transformed liver progenitor or hepatocyte/cholangiocyte-like HepaRG cells. However, exposure to the virus causes partial dedifferentiation of HepaRG cells. SARS-CoV-2 can also establish efficient replication in some low-passage, high-grade glioblastoma cell lines. In contrast, embryonal primary astrocytes or neuroblastoma cells did not support replication of the virus. Glioblastoma cell permissiveness is associated with defects in interferon production. Overall, these results suggest that liver dysfunction during COVID-19 is not due to infection of these tissues by SARS-CoV-2. Furthermore, tumors may potentially serve as reservoirs for the virus during infection.
ABSTRACT
Poultry enteritis is an important multifactorial disease. Avian coronavirus (ACV) is one of many viruses related to enteric diseases and infectious bronchitis. Aim of this study was to find out the occurrence of ACV in enteritis affected broiler, molecular detection, phylogenetic analysis of avian corona virus and to examine intestine and liver for gross and microscopic lesions. Dead poultry birds (N=604) affected with enteritis were examined for presence of ACV. Intestinal samples of four birds were pooled to make one biological sample enteric ACV as the causative agent of enteritis in commercial poultry sector in and around four major districts of Rajasthan by RT-PCR. Molecular characterization was carried out by partial gene sequencing. Liver and intestine were examined grossly during post-mortem and by histopathology. Out of 151 pooled samples tested 51 (35.10%) were found positive for ACV. Prevalence of enteric ACV was highest in Ajmer (45.94%) and lowest in Dungarpur (23.07%) districts. 0-1 weeks age chicken flocks were found more susceptible for enteric ACV with 33.80% prevalence. Comparison of ACV sequence of this study revealed nucleotide (nt) identities from 99.44% among themselves, 99.44% with ACV from abroad. The amino acid (aa) identities of ACV of this study among themselves and with abroad sequences was 47.06 to 100%. Further severe congestion in intestine and necrotic patches on liver were recorded. Histopathology showed severe villous atrophy, congestion and cystic glands in sub-mucosa in intestine and severe congestion and haemorrhages along with infiltration of inflammatory cells in liver parenchyma.
ABSTRACT
Researchers have shown that SARS-CoV and MERS-CoV can also cause liver damage in an infected organism, but the mechanisms of injury are poorly understood. In this study, pathomorphological changes in the liver during coronavirus infection in pregnant women were studied. As material, the liver was studied at autopsy of maternal mortality from 33 coronaviruses conducted at RCPA (Republican Center for Pathological Anatomy) between 2020 and 2021. Morphological examinations of liver tissue showed that the development of various pathomorphological changes in the liver was also observed depending on the periods of coronavirus infection. In the exudative period of the coronavirus is observed a strong process of circulating in the liver, swelling, destruction and bleeding of interstitial tissue, the development of protein and hydropic dystrophy in the liver parenchyma, i.e. hepatocytes. In the second proliferative inflammatory period of the disease, there is an increase in lymphoid infiltration along the portal pathways of the liver, myxomatous metaplasia of Kupffer cells, proliferation and proliferation of fibroblasts, growth of connective tissue, portal pathways of fibrous structures, periphery and even sinusoidal wall.