Yes, the SARS-Cov-2, may cause damage tissues having very little ACE2 receptors

indirectly due to ischemia, microangiopathy thrombosis, and vasculitis.

This is why it can affect any part and system of the human body.

Yes, the SARS-Cov-2, may cause damage tissues having very little ACE2 receptors

See these article

Muhammad Yousuf < the SARS-Cov-2, may cause damage tissues having very little ACE2 receptors indirectly due to ischemia, microangiopathy thrombosis, and vasculitis. >

Do you know any reference about this? I would like to read. Thanks.

Dear Yuan-Yeu Yau

These articles may help you understand tissues that have very little ACE2 receptors and impact on severity of COVID-19.

1. Article Tissue distribution of ACE2 protein, the functional receptor...

2. Article Angiotensin Converting Enzyme 2: SARS-CoV-2 Receptor and Reg...

2. Article ACE2 Receptor Expression and Severe Acute Respiratory Syndro...

Indirectly damage the other cells by tissue anoxia as described by other authors. Muhammad Yousuf provided very good articles regarding this.

Krishna kumar Ganta,

Yes, it has been reported that SARS-CoV-2 may be able to gain entry into host cells through a different receptor (other than ACE2).

A recent study (https://www.biorxiv.org/content/10.1101/2020.06.05.134114v1.full.pdf) has identified Neuropilin-1 as a host factor for SARS-CoV-2 infection.

You may also want to read the review article (Article Understanding COVID-19 - A Molecular Perspective

There is still conflicting evidence on the precise role ACE2 plays in coronavirus infections.

In some cases, it can actually be of benefit: ACE2 has been shown to reduce injury to the lung tissue in cases of the original Sars virus in mice by doing its job and causing blood vessels to dilate.

In another mouse study, however, the binding of the Sars spike protein to ACE2 was shown to contribute to lung damage.

When it comes to the current coronavirus, early studies have shown that the introduction of a human-made form of ACE2 to human cells can block the early stages of infection by binding the spike protein, preventing it from entering the cells. ACE2 thus acts both as an entry port to cells but also as a mechanism to protect the lung from injury.

Thanks everyone for the answers. I sincerely appreciate them. Here is what I found.

1) sars1 did not infect 293t cells even after transient expression of high levels of ace2 but when stablely expressed ace2 using lentivirus the sars1 infected 2931. So the questions raised are, Why did the virus not infect when the cells expressed ace2 transiently. What changes did HIV do so that sars1 entered the cells.?

2. In Two different cells expressing different levels of ace2, why did sars2 infect more in the cells expressing less ace2 compared to cells expressing high ace2? Thanks zeina for your answer.

3. Recent paper although got retracted in nature immunology for wrongly interpreting few results. But the fact they presented has strong evidences and acceptance even by people who raised questions on the paper. The fact is cov2 infected T - lymphocytes which are negative to Ace2. Only 1 percent of the patients have the virus in the blood (3 out of 275 ). They enter the blood stream in later stages and that being the reason why patients have delayed immune response. However if entered the blood they can infect T-lymphocytes. What other receptors does it use to enter a non ace2 cell.?

Thanks

Michael okpara, thanks for your answer. While in all the papers you mentioned ace2 is necessary to infect but what was interesting is the virus could use various co receptors to enhance infection.

Following, closely

Yes Krishna kumar Ganta

Suggested mechanism for that Palem Harinath