Should we worry about the long-term impact of the novel coronavirus?

It is in the nature of a microbe to multiply and cause diseases. SARS-CoV-2 is doing exactly this. While the immediate morbidity and mortality is a problem in case of this novel coronavirus, long-term impacts on health has raised concerns as well.

Over the last seven-eight months, evidence has accumulated that the virus can cause large-scale damage to the lungs, pharynx, heart, liver, brain and kidneys.

Such multi-organ damage was observed in many other viral pathogens. The Zika virus, for example, was isolated from placental tissues, both male and female reproductive tissues, nerve cells and ocular tissues such as the cornea, retina and even the optic nerve. This is, however, not a norm and other viruses like the poliovirus target just the central nervous system.

One of the primary reasons this coronavirus can accumulate in multiple organs is that the receptor or the proteins — recognised by the virus as an entry point into the cell — are widely distributed in the body. This receptor is angiotensin-converting enzyme 2, an enzyme which has the primary function of lowering blood pressure and is therefore very common on the cell membranes of lungs, arteries, heart, kidney and intestines.

This affinity of the virus to certain body tissues is called tropism and other than receptors, it is also controlled by factors such as the presence of physical barriers, local temperature and pH, which is a measure of acidity or basicity.

Rhinoviruses, for example, multiply exclusively in the upper respiratory tract because they are adapted to multiply best at low temperature and pH. Similarly, enteroviruses can multiply in the intestine because they resist inactivation by digestive enzymes, bile and acid. The factors controlling tropism are difficult to regulate through external manipulation.

Once these reach a tissue, they can damage it in two ways. Damage can be direct due to takeover of the host cell or indirect, due to processes such as inflammation and the host immune response. Other than this, the extent of damage also depends on the mode of transport that the virus uses to spread in the body.

While many viruses move around the body through the blood and lymphatic circulatory system, others piggyback on the nervous system. More debilitating diseases seem to be caused by viruses that use the nervous system.

The rabies virus, for example, enters the body through the bite of a rabid dog and after initial replication under the skin and muscle around the bite, the virus spreads through the axons and dendrites of the nerve cells and perineural cells around the nerve cells. Even polio virus and herpes virus travel through this system.

The virus benefits by using this route as it is shielded from antibodies. Damage is permanent as the cells in the central nervous system (CNS) take a lifetime to regenerate.

There is evidence that SARS-CoV-2 also moves around through the CNS. This can explain symptoms like headache, sense of smell and altered mental status. But as the virus is new, it is still not clear whether the virus can induce chronic damage to the CNS system.

Many infections lead to lifelong damage to the body. People complain of joint pain years after contracting chikungunya and dengue. Similarly, people who contract bacterial infection like the Lyme disease too report long-term impacts like cognitive dysfunction and joint pains. Pulmonary tuberculosis damages the lungs as well.

When this damage is in tissues that regenerate slowly, like in the brain, the lungs, nerve cells and cells in the eyes, it can reduce quality of life. The novel coronavirus adds to this list.

This ability to cause long-term effects on health is not limited to the novel coronavirus. But even closely related coronaviruses behave differently. SARS-CoV-2 replication in the lung, for example, is similar to SARS-CoV, but is lower than MERS-CoV. In conjunctiva, SARS-CoV-2 replication was greater than SARS-CoV.

There seems to be little we can do to reduce the adverse effects of infectious diseases. The only silver lining is that understanding these mechanisms provide targets for developing drugs to treat these viral pathogens. But drug recovery is a slow process.

So, yes, worry we should.

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