Coronavirus uses same strategy as HIV to dodge immune response, Chinese study finds
- Both viruses remove marker molecules on surface of an infected cell that are used to identify invaders, according to Chinese researchers
- This commonality could mean Sars-CoV-2 may be around for some time, they say
Both viruses remove marker molecules on the surface of an infected cell that are used by the immune system to identify invaders, the researchers said in a non-peer reviewed paper posted on preprint website bioRxiv.org on Sunday. They warned that this commonality could mean Sars-CoV-2, the clinical name for the virus, could be around for some time, like HIV.
Virologist Zhang Hui and a team from Sun Yat-sen University in Guangzhou also said their discovery added weight to clinical observations that the coronavirus was showing “some characteristics of viruses causing chronic infection”.
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Their research involved collecting killer T cells from five patients who had recently recovered from Covid-19, the disease caused by the virus. Those immune cells are generated by people after they are infected with Sars-CoV-2 – their job is to find and destroy the virus.
But the killer T cells used in the study were not effective at eliminating the virus in infected cells. When the scientists took a closer look they found that a molecule known as major histocompatibility complex, or MHC, was missing.
The molecule is an identification tag usually present in the membrane of a healthy cell, or in sick cells infected by other coronaviruses such as severe acute respiratory syndrome, or Sars. It changes with infections, alerting the immune system whether a cell is healthy or infected by a virus.
HIV uses the same strategy – MHC molecules are also absent in cells infected with that virus.
“In contrast, Sars does not make use of this function,” Zhang said.
The coronavirus removes these markers by producing a protein known as ORF8, which binds with MHC molecules, then pulls them inside the infected cell and destroys them, the researchers said.
ORF8 is known to play an important role in viral replication, and most commercial test kits target this gene to detect viral loads in nose or oral swabs.
While drugs being used to treat Covid-19 patients mainly targeted enzymes or structural proteins needed for viral replication, Zhang and his team suggested compounds be developed “specifically targeting the impairment of MHC by ORF8, and therefore enhancing immune surveillance for Sars-CoV-2 infection”.
Earlier studies have found the spike protein of the new coronavirus had a structure that allowed it to enter many types of human cells and bind with them. The same structure was also found in HIV, but not in other coronaviruses found in animals such as bats and pangolins.
Another study by researchers in New York and Shanghai also found that Sars-CoV-2 could kill T cells. The discovery came after autopsies in China found immune system destruction similar to that caused by Aids.
Four decades after HIV – a virus that attacks the immune system – emerged, it has killed about 32 million people globally, according to the World Health Organisation, and there is still no vaccine or drug that can completely cure the disease.
Zhang Shuye, principal investigator with the Shanghai Public Health Clinical Centre at Fudan University, said the findings of the Guangzhou study were “not entirely a surprise”, and unrelated viruses could take on similar traits as they came under similar selective pressure.
Suppression of MHC molecules had also happened in other viruses such as some herpes viruses, said Zhang, who was not involved in the study.
He noted that the new coronavirus was not hijacking T cells and turning them into a means to reproduce, as HIV did, adding that the new virus was mutating at a much slower pace and the death rate was “much, much lower than for Aids”.
He said the body’s immune system had various ways to fight back. “What we need to bear in mind through this pandemic is that, though the virus may have some traits that are new or unexpected, the majority of patients recover,” Zhang said. “This should give us some confidence.”