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XEC is an Omicron variant, Russo explains. But it has several mutations in the spike protein, which is what the virus uses to infect you. That can make XEC more contagious than previous variants ...
Other symptoms are less common among people with COVID-19. Some people experience gastrointestinal symptoms such as loss of appetite, diarrhea, nausea or vomiting. [1] [65] A June 2020 systematic review reported a 8–12% prevalence of diarrhea, and 3–10% for nausea. [2] Less common symptoms include chills, coughing out blood, diarrhea, and rash.
Scientists named these variants after Greek letters: alpha, beta, gamma, delta and omicron. Delta, which became dominant in the U.S. in June 2021, raised a lot of concerns because it was twice as likely to lead to hospitalization as the first version of the virus. Then in late November 2021, a new variant came on the scene: omicron.
This comes as speculation swirls that the virus might be taking up residence in the gut—versus like the upper respiratory tract, where Omicron tends to hang out, or the lower respiratory tract ...
If you do get sick, drink plenty of fluids (especially liquids with electrolytes), get plenty of rest and only eat soft, bland foods. This article was originally published on Dec. 12, 2024 and has ...
It is difficult to distinguish between symptoms caused by infection of the HCoV-NL63 virus and those caused by other common human viruses, making diagnosis and detection complex. Reverse transcription polymerase chain reaction of samples collected through nasopharyngeal swab is the most commonly used method for detection of the virus. [ 10 ]
These make it more difficult for antibodies to neutralise the virus." [ 260 ] A 2024 study published in JAMA Network Open found that vaccinated individuals infected with the Omicron or Delta variants of COVID-19 did not have a higher overall risk of developing new autoimmune diseases compared to those who were not infected. [ 261 ]
Virus infections start when viral particles bind to host surface cellular receptors. [158] Protein modeling experiments on the spike protein of the virus soon suggested that SARS‑CoV‑2 has sufficient affinity to the receptor angiotensin converting enzyme 2 (ACE2) on human cells to use them as a mechanism of cell entry. [159]