The UC Riverside study has the potential to help scientists develop strategies to prevent the spread of COVID-19 among minks and other species. Research has revealed that the way SARS-CoV-2, the virus that causes COVID-19, enters mink cells is different from that of human cells. Because the TMPRSS2 enzyme in minks is inactive, it uses the endocytic pathway. This finding highlights the complexity of zoonotic diseases and the potential public health risk of cross-species transmission of viruses, emphasizing the need for further research in different species.
Some viruses have the ability to spread across species. SARS-CoV-2, the virus that causes COVID-19, is an obvious example. The virus can be transmitted from humans to minks (an agricultural species) and then possibly to humans. This phenomenon, known as "spillover," has raised concerns because the virus could mutate in minks and then return to humans in a more aggressive form. Transmission from humans to mink (spillover) and from mink to humans (spillover) has been documented in mink farms in the United States and Europe.
To address these questions, a University of California, Riverside, research team has now studied zoonoses—the interspecies transmission of pathogens—in minks and found that TMPRSS2—an enzyme critical for the human SARS-CoV-2 virus to fuse into the human body—does not work in mink.
"We found that mink lung cells are infected through the 'endocytic pathway' rather than the TMPRSS2 fusion pathway commonly seen in human cells," said doctoral candidate Ann Song, first author of the research paper published in Frontiers in Microbiology. "Our results show that SARS-CoV-2 does not enter the same way in all mammals, highlighting the need for in-depth studies of viral entry mechanisms in different species.
Song explained that viral fusion occurs when the viral membrane fuses with the host cell's plasma membrane during infection. Endocytosis is an important process in which cells engulf foreign materials through small vesicles formed in their plasma membrane, she said. Host cells can absorb the SARS-CoV-2 virus through endocytosis, she said.
"Our results show that the functional domain (or enzymatic domain) is missing in mink TMPRSS2. We don't know why. We think this enzyme may have multiple functions. It can play other roles in mink, but it does not play a role in the fusion of SARS-CoV-2 with host cells. Therefore, targeting TMPRSS2 will not help prevent infection in mink. It is obvious that SARS-CoV-2 enters different species and tissue types differently," she said.
Zoonoses are a public health concern because dangerous mutant viruses can enter humans through spillover. During the pandemic, hundreds of papers were published on COVID-19 in humans. Now that the spread of COVID-19 in humans is better controlled, the scientific community’s attention is turning to zoonotic diseases.
Lead author Prue Talbot, a graduate professor in the Department of Molecular, Cellular and Systems Biology, said researchers should not underestimate the possibility of SARS-CoV-2 spillover and spillover in other mammalian species: "Lethal mutants may emerge from spillover/spillover events. Another example is that many deer herds hunted by humans are infected with SARS-CoV-2 and are therefore potential sources of spillover."
Postdoctoral researcher Rattapol Phandthong also joined Talbot and Song's research team. Next, the research team will study the infectivity of human embryos from pregnant women infected with COVID-19.
To achieve their findings, the researchers conducted experiments using mink lung epithelial cells.
Compiled source: ScitechDaily