Thursday, May 28, 2020

Who In The World Would Concoct Something Like Airborne HIV?



SCMP  |  The novel coronavirus uses the same strategy to evade attack from the human immune system as HIV, according to a new study by Chinese scientists.

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”.

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.

biorxiv |   SARS-CoV-2 infection have caused global pandemic and claimed over 5,000,000 tolls14. Although the genetic sequences of their etiologic viruses are of high homology, the clinical and pathological characteristics of COVID-19 significantly differ from SARS5,6. Especially, it seems that SARS-CoV-2 undergoes vast replication in vivo without being effectively monitored by anti-viral immunity7. Here, we show that the viral protein encoded from open reading frame 8 (ORF8) of SARS-CoV-2, which shares the least homology with SARS-CoV among all the viral proteins, can directly interact with MHC-I molecules and significantly down-regulates their surface expression on various cell types. In contrast, ORF8a and ORF8b of SARS-CoV do not exert this function. In the ORF8-expressing cells, MHC-I molecules are selectively target for lysosomal degradation by an autophagy-dependent mechanism. As a result, CTLs inefficiently eliminate the ORF8-expressing cells. Our results demonstrate that ORF8 protein disrupts antigen presentation and reduces the recognition and the elimination of virus-infected cells by CTLs8. Therefore, we suggest that the inhibition of ORF8 function could be a strategy to improve the special immune surveillance and accelerate the eradication of SARS-CoV-2 in vivo.