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As millions of others recover from COVID-19, an unanswered consultation is to what extent the virus can “hide” in individuals who were supposedly recovered. If so, can some of the persistent symptoms of COVID-19 be or pose a threat of transmission of the infection to others even after recovery?
I am a medical scientist of infectious diseases at the University of Virginia, where I treat inflamed patients and conduct studies on COVID-19. Here, I will briefly review what is known about chronic or persistent COVID-19.
Chronic or persistent infection continues for months or even years, during which the virus occurs frequently, although in many cases at low levels. Often, these infections occur at an immune site called privileged.
There are some options in the framework that are less available for the immune formula and where it is difficult to eliminate all viral infections. These come with the central nerve formula, testicles and eyes. It is idea that the evolutionary merit of having an immune region that you like is that it protects a brain similar, for example, from the damage caused by inflammation that occurs when the immune formula fights an infection.
An immune system you like is not only difficult for the immune formula to penetrate, but also limits proteins that accumulate inflammation. The explanation is why if inflammation is helping to kill a pathogen, it can also damage an organ such as the eye, brain or testicles. The result is a complicated truce where inflammation is limited but the infection continues to worsen.
But there is a way for a virus to hide in the frame and reappear later.
A latent viral infection occurs when the virus is delivered to an inflamed mobile device, but sleeps and does not multiply. In a latent virus, the entire viral genome is provided and an infectious virus can occur if latency ends and infections are active. The latent virus can be integrated into the human genome, such as HIV, or it may exist in the nucleus in the form of a self-replicating DNA fragment called an episome.
A latent virus can reactivate and cause infectious viruses, and this can occur months or decades after the initial infection. Perhaps the most productive example is chickenpox, which is said to have been eliminated through the immune system, can be reactivated and cause shingles decades later. Fortunately, chickenpox and shingles are now prevented by vaccination. Being inflamed with a virus capable of generating a latent infection is to be inflamed for the rest of your life.
Herpes viruses are through maximum non-unusual viral infections that identify latency.
It is a giant circle of relatives of viruses whose genetic material, or genome, is encoded through DNA (not RNA as the new coronavirus). Herpes viruses come not only with herpes simplex 1 and 2 viruses, which cause oral and genital herpes, but also chickenpox. Other herpes viruses, such as the epstein Barr virus, which causes mononucleosis, and cytomegalovirus, which is a specific challenge in immunocompromised people, can also arise after latency.
Retroviruses are another unusual circle of virus relatives who identify latency but through a different mechanism to the herpes virus. Retroviruses such as HIV, which causes AIDS, can insert a copy of your genome into human DNA that is a component of the human genome. There, the virus can exist indefinitely in the dormant state in inflamed humans, as the virus genome is copied each time DNA is replicated and a mobile is divided.
Viruses that identify latency in humans are difficult, if not impossible, to eliminate for the immune system. In fact, latency, there would possibly be little or no viral protein production in the inflamed cell, making the infection invisible to the immune system. Fortunately, coronaviruses do not identify a latent infection.
In a small study, the new coronavirus was detected in semen in a quarter of patients with an active infection and in less than 10% of patients who were supposedly recovered. In this study, viral RNA was what was detected, and it is not yet known whether this RNA came from a virus that was still infectious or died in semen; and if it’s alive, if the virus can be sexually transmitted. So many vital questions remain unanswered.
Ebola is a very different virus from SARS-C0V-2, but serves as an example of viral patience on immune sites. In some individuals, Ebola survives on privileged immune sites for months after acute disease resolves. Ebola survivors have been documented with persistent infections in the testicles, eyes, placenta and central nervous system.
WHO recommends that male Ebola survivors check the virus every 3 months. They also recommend that couples refrain from having sex for 12 months after recovery or until their sperm is twice negative for Ebola. As noted above, we want to know more about new persistent coronavirus infections before we can make similar recommendations.
CoVID-19 recovery is delayed or incomplete in many people, with symptoms such as coughing, shortness of breath and fatigue. These constitutional symptoms are unlikely to be caused by viral patience because the symptoms do not come from preferred immune sites.
Other sites where a coronavirus has been detected come with the placenta, intestines, blood and, of course, the airways. In women who contract COVID-19 pregnancy, the placenta develops defects in the mother’s blood vessels that feed the placenta. However, its importance in fetal fitness remains to be determined.
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The new coronavirus can also infect the fetus and placenta. Finally, the new coronavirus is also provided in the blood, nasal hollow space and palate for up to a month or more after infection.
Evidence is being developed to recommend that SARS-CoV-2 can infect liked immune sites and, from there, cause persistent but non-latent chronic infections. It is too early to know to what extent these persistent infections affect a person’s health, such as the pregnant mother, or to what extent they contribute to the spread of COVID-19.
William Petri, Professor of Medicine, University of Virginia
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