Please subscribe today to NJ. Katherine Rodriguez can be reached at krodriguez njadvancemedia. Have a tip? Tell us at nj. Note to readers: if you purchase something through one of our affiliate links we may earn a commission. For Abby Knowles, a headache and fatigue was just the start. She soon felt like she had a tight band across her chest, making it difficult to breathe. Her blood pressure began to oscillate — too low, too high — leaving her lightheaded and nauseous.
A symptom might taper off, only to return. Meanwhile, her husband Dan, who also became sick toward the end of March, had a high fever and more typical COVID symptoms for a few days but soon recovered. The experiences of the Knowles and many COVID patients point to the ways that the coronavirus can be maddeningly unpredictable.
Some people have debilitating illness, while others barely feel sick, if at all. Some patients are struggling to get back to normal long after being sick. And the way the disease plays out by age can be baffling. That group generally tends to fare better than the very young and very old with viral infections one glaring exception: the flu pandemic, which killed healthy, young adults at a high rate.
During a viral infection, the infected cells put out a call to arms and a call for reinforcements, says virologist Benjamin tenOever of the Icahn School of Medicine at Mount Sinai in New York City.
The cells also send out proteins called chemokines, which attract immune cells to the site of infection. Viruses endeavor to overcome both calls.
SARS-CoV-2 does something different: It slams the brakes on the call to arms but puts the gas on the call for reinforcements, tenOever says. In experiments with cells, animals and blood and tissue samples from COVID patients, tenOever and his colleagues found low levels of interferons, which sound the call to arms. But levels of chemokines , which bring in the cavalry of immune cells, were high, the researchers report May 28 in Cell.
The excessive show of immune cell force spurs inflammation and cell death, which can stoke yet more inflammation and cell death. This severe immune reaction can damage the lungs and other organs. The way that SARS-CoV-2 tangles with the immune system largely sets it apart from other viruses, although SARS-CoV — the coronavirus behind the Severe Acute Respiratory Syndrome outbreak in — also showed the same mismatched approach to the call to arms and call for reinforcements, tenOever says.
Our data revealed that the MDV protein contributes to the rapid onset of Marek's disease but is not essential for virus replication, spread, and tumor formation. The virus causes immense economic losses in the poultry industry due to the high morbidity and mortality, but also the cost of the vaccination.
MDV encodes over genes that are involved in various processes of the viral life cycle.
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