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COVID Isn't Just Infecting You - It Could Be Reactivating Viruses That Have Been Dormant In Your Body For Years

From fortune.com - December 28, 2022 3:36 PM

“Long COVID” in some may not be an entirely new entity, researchers say. COVID can cause reservoirs of some viruses you’ve previously battled to reactivate, potentially leading to symptoms of chronic fatigue syndrome—a condition that resembles long COVID, a recent study found. You had COVID a few months ago and recovered—but things still aren’t quite right. When you stand up, you feel dizzy, and your heart races. Even routine tasks leave you feeling spent. And what was once a good night’s sleep no longer feels refreshing. Long COVID, right? It may not be so simple. A mild or even an asymptomatic case of COVID can cause reservoirs of some viruses you’ve previously battled to reactivate, potentially leading to symptoms of chronic fatigue syndrome—a condition that resembles long COVID, according to a recent study published in the journal Frontiers in Immunology. Researchers found herpes viruses like Epstein-Barr, one of the drivers behind mono, circulating in unvaccinated patients who had experienced COVID. In patients with chronic fatigue syndrome, antibody responses were stronger, signaling an immune system struggling to fight off the lingering viruses.

Such non-COVID pathogens have been named as likely culprits behind chronic fatigue syndrome, also known as myalgic encephalomyelitis. The nebulous condition with no definitive cause leads to symptoms like fatigue, brain fog, dizziness when moving, and unrefreshing sleep. The symptoms of many long COVID patients could be described as chronic fatigue syndrome, experts say. Researchers in the October study hypothesized that COVID sometimes leads to suppression of the immune system, allowing latent viruses reactivated by the stress of COVID to recirculate—viruses linked to symptoms that are common in Chronic Fatigue Syndrome and long COVID. Thus, “long COVID” in some may not be an entirely new entity, but another postviral illness—like ones seen in some patients after Ebola, the original SARS of 2003–2004, and other infections—that overlaps with chronic fatigue syndrome. As top U.S. infectious disease expert Dr. Anthony Fauci said in 2020, long COVID “very well might be a postviral syndrome associated with COVID-19.”

‘We’re still not doing that’

It’s possible that COVID is reactivating latent viruses in at least a portion of long COVID patients, causing chronic fatigue syndrome symptoms, Dr. Alba Miranda Azola, codirector of the long COVID clinic at Johns Hopkins University School of Medicine, told Fortune. But her clinic doesn’t check for the reactivation of viruses in long COVID patients. She doesn’t think the possibility of such viruses causing symptoms in patients is worth giving those patients antivirals or antibiotics, which can lead to undesirable side effects. “We don’t have enough evidence to support that treatment,” she said. Other physicians who have prescribed such treatments for long COVID patients, and those patients didn’t see much improvement, Azola added. She recently asked an infectious disease colleague if it was standard practice to test for, and treat, latent viruses in long COVID patients. “We’re still not doing that,” she recalled him saying. Dr. Nir Goldstein, a pulmonologist at National Jewish Health in Denver, who runs the hospital’s long COVID clinic, said it’s not yet clear what role latent viruses play in the long COVID. That’s because the nascent condition is such a complex and varied disorder. A consensus definition for long COVID hasn’t been universally agreed upon. Hundreds of possible symptoms have been identified, he points out—and no single explanation can account for them all.

“There may be an association, but it’s very hard to know the causation,” Goldstein said. “It could be the other way around—it could be that long COVID causes reactivation, not that reactivation causes long COVID.” Dr. Panagis Galiasatos, an assistant professor at Johns Hopkins’ pulmonary and critical care division who treats long COVID patients, doesn’t routinely test his patients for latent viruses, given that most respond well to treatments that his clinic uses. “If a patient doesn’t respond to treatment, maybe we’ll test for other things,” he said. There is a strong possibility that COVID is weakening the immune systems of “a good deal of people,” Galiasatos added. “I do think the immunodeficiency—when it’s there, it’s transient—allows those viruses to reemerge,” he said. Scientists are still unsure if viruses like Epstein-Barr merely initiate chronic fatigue syndrome or keep symptoms going, the October study points out. Similarly, researchers are still unsure what, if any, role latent viruses—including, potentially, SARS-CoV-2 itself—play in the development of long COVID.

Few options, for now

With so little known about both long COVID and chronic fatigue syndrome, it doesn’t really matter which a patient has, experts say—at least not right now. While the symptoms of both can be treated, there’s no specific drug for either because the cause—or causes—remain up in the air. “It’s the main reason why I don’t even order the test,” Azola said of antibody tests for possible latent viruses in long COVID patients. “There’s no treatment targeting chronic fatigue syndrome. There certainly are treatments that can help with symptom management and improve quality of life, but they’re not curative.” Delineating the two conditions could matter in the future, Goldstein said, if researchers can prove that the conditions are caused by residual viruses and develop a way to eradicate them. Azola has several patients who were diagnosed with chronic fatigue syndrome before COVID, after Epstein-Barr virus or H1N1 flu infections. They caught COVID, and now their chronic fatigue symptoms are much worse, she says. “They remember the things that worked for them before, learning how to pace themselves, staying out of what I call the corona-coaster—when they’re feeling good, doing a lot, then crashing for days,” she said. “They’re able to identify with that and implement strategies that have worked for them in the past.” Galiasatos, from Johns Hopkins, hopes that the new year brings long COVID breakthroughs, including a deeper understanding of the condition and tailored treatments—potentially by the end of 2023. Stanford University is recruiting for a study based on a theory similar to the one in the October study—that long COVID is caused by a lingering reservoir of the SARS-CoV-2 virus, which causes COVID, after acute infection. It will attempt to determine if the antiviral drug Paxlovid alleviates long COVID symptoms by reducing or eliminating that viral reservoir. “We’re starting to move into the trial-treatment phase slowly,” Azola said.

Study Cited Published in Frontiers in Immunology:

https://doi.org/10.3389/fimmu.2022.949787

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Clarisse Staehlé's curator insight, January 2, 2023 12:42 PM

Les chercheurs ont découvert que le virus d’Epstein-Barr pourrait être réactivé lors d’une infection au COVID-19.

Chez les patients atteints du syndrome de fatigue chronique, les réponses en anticorps étaient plus fortes, signalant un système immunitaire luttant pour combattre les virus persistants.

Il n’y a pas suffisamment de preuves qui permettrait de développer un traitement.

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Episodes of Herpes virus Reactivation More Common in Astronauts - NASA study

From www.healio.com - August 2, 2019 11:41 AM

Latent herpes virus reactivation has been documented in more than half of astronauts during space shuttle and International Space Station missions, and according to a recent study funded by NASA, the cause is stress.“Herpes virus is a broad category of viruses, beyond the small subset that cause sexually transmitted diseases.Most humans become infected early in life with one or more, and never fully clear these viruses,” Satish Mehta, PhD, senior scientist in the immunology/virology lab at the Johnson Space Center in Houston, told Infectious Disease News.

Results showed that 47 out of 89 (53%) astronauts on short space shuttle flights, and 14 out of 23 (61%) on longer space station missions shed herpes viruses in their saliva or urine samples. According to the study, astronauts shed four of the eight major human herpes viruses: Epstein-Barr, varicella-zoster and herpes simplex-1 in saliva and cytomegalovirus in urine. The researchers said most astronauts were asymptomatic, with only six developing symptoms.

“Larger quantities and increased frequencies for these viruses were found during spaceflight as compared to before or after flight samples and their matched healthy controls,” Mehta and colleagues wrote. Mehta explained why: “[The] short answer is stress. In people with reduced immunity, such as the elderly or stressed individuals, these viruses can awaken and cause disease,” he said.

“Although NASA believes there is no clinical risk to astronauts during orbital spaceflight, there is concern that during deep space exploration missions, there may be clinical risks related to viral shedding. Although we do not have a serious clinical problem related to herpes viruses, their reactivation is an excellent ‘flag,’ or biomarker, for stress and reduced immunity.”

In the study, Mehta and colleagues noted that continued viral shedding after a flight can pose a potential risk for crew who may encounter infants, seronegative adults or immunocompromised people, so protocols have been put in place.

The study was published in February 2019 in Frontiers in Microbiology - Virology:

https://doi.org/10.3389/fmicb.2019.00016

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Clarisse Staehlé's curator insight, November 25, 2022 10:42 AM

A study was conducted by NASA on astronauts.

They showed that astronauts excrete EBV.

It is found in the saliva or urine of :

-53% of astronauts during short missions

-61% of astronauts during long missions

The virus is more present the longer the mission.

Stress is a factor linked to the increase in the frequency of the virus. This discovery has led to the implementation of a quarantine for astronauts at the end of the mission in order to avoid contaminating their relatives and people at risk.

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Reactivation of Latent HIV Moves Shock-and-Kill Treatments Forward

From www.nature.com - December 28, 2020 9:37 AM

Treatments that can reactivate latent HIV and SIV in animals. HIV-1 can evade the immune system by hiding out in a dormant form. Two studies describe interventions that can effectively reactivate the latent virus in animals, potentially rendering it vulnerable to immune-mediated death. ‘Shock and kill’ might sound like a military strategy, but in fact it describes the dominant model currently used in the search for a cure for HIV-1 infection. Although antiretroviral therapy (ART) is highly effective at limiting the extent of the infection, the virus can hide out in a ‘latent’ form in immune cells called CD4+ T cells, undergoing little or no transcription and thus remaining undetected by the immune system1,2. When ART is stopped, these viral-reservoir cells can rapidly fuel HIV rebound. The theory behind ‘shock and kill’ involves the use of drugs that reverse this latency and could increase viral gene expression (shock), rendering the viral-reservoir cells vulnerable to elimination (kill) by other cells of the immune system. Writing in Nature, two groups3,4 describe distinct interventions in animal models that cause what seem to be the most robust and reproducible disruptions of viral latency reported so far.

‘Shock and kill’ might sound like a military strategy, but in fact it describes the dominant model currently used in the search for a cure for HIV-1 infection. Although antiretroviral therapy (ART) is highly effective at limiting the extent of the infection, the virus can hide out in a ‘latent’ form in immune cells called CD4+ T cells, undergoing little or no transcription and thus remaining undetected by the immune system1,2. When ART is stopped, these viral-reservoir cells can rapidly fuel HIV rebound. The theory behind ‘shock and kill’ involves the use of drugs that reverse this latency and could increase viral gene expression (shock), rendering the viral-reservoir cells vulnerable to elimination (kill) by other cells of the immune system. Writing in Nature, two groups3,4 describe distinct interventions in animal models that cause what seem to be the most robust and reproducible disruptions of viral latency reported so far. The authors demonstrated that AZD5582 treatment led to marked increases in the levels of viral RNA in CD4+ T cells in a range of tissues in both species, indicating that transcription of the virus had been activated. This was combined with a substantial rise in virus levels in the blood. AZD5582 is not optimized for use in humans; nonetheless, these results suggest that pharmacological activation of the non-canonical NF-κB pathway could be an attractive way to trigger HIV-1-gene expression as part of a shock-and-kill approach (Fig. 1).

In the second study, McBrien et al.4 used an entirely different, though complementary, approach to disrupting viral latency. Again, the authors used both ART-treated humanized mice infected with HIV-1 and ART-treated, SIV-infected rhesus macaques. They combined two immunological interventions. The first involves antibody-mediated depletion of CD8+ T cells — immune cells previously shown to act in concert with ART to reduce levels of viral transcription5. The second, administered concurrently, involves treatment with a drug called N-803, which strongly activates the signalling molecule interleukin-15 (IL-15), and which has been previously shown6 to activate HIV-1 transcription in vitro. Like Nixon and colleagues, the researchers found that their treatment caused substantial increases in virus levels in the blood, and in viral RNA in cells from various tissues. At first glance, the combined interventions used by McBrien and colleagues might seem contradictory, because IL-15 is one of the strongest activators of CD8+ T cells7,8. But the synergistic effects of these two interventions raise the provocative possibility that the best strategies for targeting viral-reservoir cells involve a mix of immune interventions — suppressing immune components that seem to have a role in stabilizing viral latency (such as CD8+ T cells) while activating others that can effectively disrupt latency (such as IL-15 signalling)....

Published in Nature (Jan. 22, 2020):

https://doi.org/10.1038/d41586-020-00010-x

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