Cruise passengers boarding off the Argentine coast in mid-March did not know they were living at a COVID-19 access point for more than a week after shipping departed.
The explanation for why those passengers were unconscious?Because most of the cruiser’s boxes were asymptomatic.
Researchers now point to this cruise ship epidemic, in which all passengers gained surgical masks, as evidence that universal masking can result in a higher proportion of asymptomatic cases of COVID-19. Other outbreaks of more commonly asymptomatic cases where widespread masking has been implemented, in places such as prisons and meat packaging plants, provide epidemiological knowledge that masks can only reduce the viral inoculum and minimize the severity of the disease.
In the New England Journal of Medicine, Monica Gandhi, MD, and George Rutherford, MD, of the University of California, San Francisco, hypothesized that widespread population masking would possibly act as a type of “variolation. “Array exposing Americans to a smaller amount of viral waste and generating an immune response.
Gandhi told MedPage Today that the viral inoculum, or the initial dose of virus taken by a patient, is most likely a determining factor in the final severity of the disease. This is different from the patient’s next viral load, the virus replication rate measured in copies via mL.
Speculation of “variolation” holds that, at a certain level, the inoculum overwhelms the immune system and leads to serious disease. With less of this (and the threshold would possibly vary from user to user), the individual effectively fights the infection, with mild clinical illness or not.
“Diseases in which their immune formula plays an important role in poor health (and their immune formula contributes to pathogenesis) do not seem to be able to deal with a wonderful viral inoculum,” Gandhi said in an interview.
A severe COVID-19 can be caused by a reaction known as a cytokine storm, an immune reaction in which the framework attacks its own cells and tissues than the virus itself, although this theory has yet to be proven (and other theories, such as storm bradykinin, have been suggested), a maximum initial dose of SARS-CoV-2 may be the trigger.
Trials that give humans other doses of viral RNA are evidently unethical, but animal studies provide initial evidence that the viral inoculum may have an effect on the severity of the disease, Gandhi noted. inflamed people with a higher dose of SARS-CoV-2 had worse effects than those inflamed with smaller amounts of viruses.
Masked hamsters were also shown to be less likely to expand COVID-19 disease than those wearing no masks, according to a separate study, and if given the disease, it is more benign.
“We know that a superior inoculum of an infectious agent makes other people sicker,” said Peter Katona, MD, an infectious disease specialist and professor at the University of California, Los Angeles.
While there are emerging studies that viral inoculum would possibly play a role in the severity of the disease in COVID-19, other infectious disease specialists have explored how viral load, the amount of viral RNA provided in the bloodstream, can also be a disease factor. . Gravity.
At The Lancet Respiratory Medicine, an organization led through Carlos Cordon-Cardo, MD, PhD, of the Icahn School of Medicine in Mount Sinai, New York, reported that the viral load of patients who died of COVID-19 disease was particularly compatible with those of surviving patients (average log10 6. 4 copies consisting of ml versus 5. 2 copies consisting of ml , respectively). In addition, for each additional unit of viral RNA detected, researchers observed a 7% increase in the risk of mortality.
An earlier study published in The Lancet Infectious Diseases also found that the average viral load in severe cases of coronavirus is more than 60 times higher than that of mild cases, according to Yang Liu, MD, of Nanchang University in China, and his colleagues.
The Cordon-Cardo organization wrote that while classifying patients with COVID-19 remains a challenge, “transforming qualitative testing into a quantitative measure of viral load will help doctors stratify patients’ dangers and decide which treatments and trials will be conducted. “
Ravina Kullar, PharmD, MPH, an infectious disease expert and epidemiologist speaking on behalf of the Society of Infectious Diseases of America, said the question of how providers treat patients with maximum viral load is crucial.
Patients with a higher viral load “should potentially get steroid dexamethasone from the start, than an antiviral, to help save this cytokine typhoon that can lead to worse results,” Kullar said.
But studies on whether patients with higher levels of viruses will revel in worse or inconclusive results. A South Korean-based study published in JAMA Internal Medicine found that viral load was no different in asymptomatic patients compared to those with symptoms.
Although experts have evidence that viral load would possibly involve the severity of COVID-19, they also do not believe that this is the only thing contributing to a serious illness.
“I think it all depends on someone’s immune system,” Kullar said. “Viral load is a component of the image, but it’s not the full picture. “
Patients who are older, have pre-existing situations such as cardiovascular disease or cancer, or deficiencies in the immune formula, are still at risk of serious disease and viral load may not be an accurate predictor.
Katona said many unanswered questions remain about the viral load and severity of the disease: its link to transmissibility, for example, as well as how to measure it (saliva samples versus nasopharynx).
“We know some of the unknowns, but there are also many unknown unknown unknowns,” Katona said. “I’m convinced that viral load makes all the difference. We just couldn’t show it consistently. “
Amanda D’Ambrosio is a journalist on MedPage Today’s research and research team, covers obstetrics and gynecology and new clinics, and writes articles about the American fitness care system.
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