I woke up in the middle of the night with a slightly sore throat like a week ago but then it was mostly gone by the morning and then the next day I was fine. So I dunno.
Husband came up as 99.5 on a forehead scan taking small female OddSox to the dentist, and I just took my temp AND ITâS ALSO 99.5.
IS IT THE COVIDS?!??
English side thrown out. Must. Use.. Spanish instructions.
Hola. ÂĄBuenos dĂas! ÂżTe sientes enfermo? ÂĄEspero que no!
Se supone que no debes orinar en Ă©l.
Had to Google cheat that one, so it might not be what i mean.
LOL
I donât know how to not feel everything after discovering you have a borderline soul-fever with your mate during a pandemic.
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can only read the beginning of it.
iâm guessing some people are naturally immune, but a lot of us virgins is just luck, like me. i doubt iâm immune.
this dude i know took zero precautions and was going bar hopping all over the country in the middle of the pandemic. he shared drinks with my sister in AC where she came home with covid and he did not.
that dude is probably naturally immune. people like me itâs a combination of luck and not having much of a life.
This might help
Last Christmas, as the Omicron variant was ricocheting around the United States, Mary Carrington unknowingly found herself at a superspreader eventâan indoor party, packed with more than 20 people, at least one of whom ended up transmitting the virus to most of the gatheringâs guests.
After two years of avoiding the coronavirus, Carrington felt sure that her time had come: Sheâd been holding her great-niece, who tested positive soon after, âand she was giving me kisses,â Carrington told me. But she never caught the bug. âAnd I just thought, Wow, I might really be resistant here.â She wasnât thinking about immunity,which she had thanks to multiple doses of a COVID vaccine. Rather, perhaps via some inborn genetic quirk, her cells had found a way to naturally repel the pathogenâs assaults instead.
FOLLOW THE ATLANTIC
Carrington, of all people, understood what that would mean. An expert in immunogenetics at the National Cancer Institute, she was one of several scientists who, beginning in the 1990s, helped uncover a mutation that makes it impossible for most strains of HIV to enter human cells, rendering certain people essentially impervious to the pathogenâs effects. Maybe something analogous could be safeguarding some rare individuals from SARS-CoV-2 as well.
Read: America is running out of âCOVID virginsâ
The idea of coronaviral resistance is beguiling enough that scientists around the world are now scouring peopleâs genomes for any hint that it exists. If it does, they could use that knowledge to understand whom the virus most affects, or leverage it to develop better COVID-taming drugs. For individuals who have yet to catch the contagionâa fast-dwindling proportion of the populationâresistance dangles âlike a superpowerâ that people canât help but think they must have, says Paula Cannon, a geneticist and virologist at the University of Southern California.
As with any superpower, though, bona fide resistance to SARS-CoV-2 infection would likely âbe very rare,â says Helen Su, an immunologist at the National Institutes of Allergy and Infectious Disease. Carringtonâs original hunch, for one, eventually proved wrong: She recently returned from a trip to Switzerland and found herself entwined with the virus at last. Like most people who remained unscathed until recently, Carrington had done so for two and a half years through a probable combination of vaccination, cautious behavior, socioeconomic privilege, and luck. Itâs entirely possible that inborn coronavirus resistance may not even existâor that it may come with such enormous costs that itâs not worth the protection it theoretically affords.
Of the 1,400 or so viruses, bacteria, parasites, and fungi known to cause disease in humans, Jean-Laurent Casanova, a geneticist and an immunologist at Rockefeller University, is certain of only three that can be shut out by bodies with one-off genetic tweaks: HIV, norovirus, and a malaria parasite.
The HIV-blocking mutation is maybe the most famous. About three decades ago, researchers, Carrington among them, began looking into a small number of people who âwe felt almost certainly had been exposed to the virus multiple times, and almost certainly should have been infected,â and yet had not, she told me. Their superpower was simple: They lacked functional copies of a gene called CCR5, which builds a cell-surface protein that HIV needs in order to hack its way into T cells, the virusâs preferred human prey. Just 1 percent of people of European descent harbor this mutation, called CCR5-Î32, in two copies; in other populations, the trait is rarer still. Even so, researchers have leveraged its discovery to cook up a powerful class of antiretroviral drugs, and purged the virus from two people with the help of Î32-based bone-marrow transplantsâthe closest that medicine has come to developing a functional HIV cure.
The stories with those two other pathogens are similar. Genetic errors in a gene called FUT2, which pastes sugars onto the outsides of gut cells, can render people resistant to norovirus; a genomic tweak erases a protein called Duffy from the walls of red blood cells, stopping Plasmodium vivax,one of several parasites that causes malaria, from wresting its way inside. The Duffy mutation, which affects a gene called DARC/ACKR1, is so common in parts of sub-Saharan Africa that those regions have driven rates of P. vivax infection way down.
In recent years, as genetic technologies have advanced, researchers have begun to investigate a handful of other infection-resistance mutations against other pathogens, among them hepatitis B virus and rotavirus. But the links are tough to definitively nail down, thanks to the number of people these sorts of studies must enroll, and to the thorniness of defining and detecting infection at all; the case with SARS-CoV-2 will likely be the same. For months, Casanova and a global team of collaborators have been in contact with thousands of people from around the world who believe they harbor resistance to the coronavirus in their genes. The best candidates have had intense exposures to the virusâsay, via a symptomatic person in their homeâand continuously tested negative for both the pathogen and immune responses to it. But respiratory transmission is often muddied by pure chance; the coronavirus can infiltrate people silently, and doesnât always leave antibodies behind. (The team will be testing for less fickle T-cell responses as well.) People without clear-cut symptoms may not test at all, or may not test properly. And all on its own, the immune system can guard people against infection, especially in the period shortly after vaccination or illness. With HIV, a virus that causes chronic infections, lacks a vaccine, and spreads through clear-cut routes in concentrated social networks, âit was easier to identify those individualsâ whom the virus had visited but not put down permanent roots within, says Ravindra Gupta, a virologist at the University of Cambridge. SARS-CoV-2 wonât afford science the same ease of study.
Read: Is BA.5 the âreinfection wave?â
A full analogue to the HIV, malaria, and norovirus stories may not be possible. Genuine resistance can manifest in only so many ways, and tends to be born out of mutations that block a pathogenâs ability to force its way into a cell, or xerox itself once itâs inside. CCR5, Duffy, and the sugars dropped by FUT2, for instance, all act as microbial landing pads; mutations rob the bugs of those perches. If an equivalent mutation exists to counteract SARS-CoV-2, it might logically be found in, say, ACE2, the receptor that the coronavirus needs in order to break into cells, or TMPRSS2, a scissors-like protein that, for at least some variants, speeds the invasive process along. Already, researchers have found that certain genetic variations can dial down ACE2âs presence on cells, or pump out junkier versions of TMPRSS2âhints that there could be tweaks that further strip away the molecules. But âACE2 is very importantâ to blood-pressure regulation and the maintenance of lung-tissue health, said Su, of NIAID, whoâs one of many scientists collaborating with Casanova to find SARS-CoV-2 resistance genes. A mutation that keeps the coronavirus out might very well âmuck around with other aspects of a personâs physiology.â That could make the genetic tweak vanishingly rare, debilitating, or even, as Gupta put it, ânot compatible with life.â People with the CCR5-Î32 mutation, which halts HIV, âare basically completely normal,â Cannon told me, which means âHIV kind of messed up in âchoosingâ CCR5.â The coronavirus, by contrast, has figured out how to exploit something vital to its hostâan ingenious invasive move.
The superpowers of genetic resistance can have other forms of kryptonite. A few strains of HIV have figured out a way to skirt around CCR5, and glom on to another molecule, called CXCR4; against this version of the virus, even people with the Î32 mutation are not safe. A similar situation has arisen with Plasmodium vivax, which âwe do see in some Duffy-negative individuals,â suggesting that the parasite has found a back door, says Dyann Wirth, a malaria researcher at Harvardâs School of Public Health. Evolution is a powerful strategyâand with SARS-CoV-2 spewing out variants at such a blistering clip, âI wouldnât necessarily expect resistance to be a checkmate move,â Cannon told me. BA.1, for instance, conjured mutations that made it less dependent on TMPRSS2 than Delta was.
Read: The BA.5 wave is what COVID normal looks like
Still, protection doesnât have to be all or nothing to be a perk. Partial genetic resistance, too, can reshape someoneâs course of disease. With HIV, researchers have pinpointed changes in groups of so-called HLA genes that, through their impact on assassin-like T cells, can ratchet down peopleâs risk of progressing to AIDS. And a whole menagerie of mutations that affect red-blood-cell function can mostly keep malaria-causing parasites at bayâthough many of these changes come with âa huge human cost,â Wirth told me, saddling people with serious clotting disorders that can sometimes turn lethal themselves.
With COVID-19, too, researchers have started to home in on some trends. Casanova, at Rockefeller, is one of several scientists who has led efforts unveiling the importance of an alarm-like immune molecule called interferon in early control of infection. People who rapidly pump out gobs of the protein in the hours after infection often fare just fine against the virus. But those whose interferon responses are weak or laggy are more prone to getting seriously sick; the same goes for people whose bodies manufacture maladaptive antibodies that attack interferon as it passes messages between cells. Other factors could toggle the risk of severe disease up or down as well: cellsâ ability to sense the virus early on; the amount of coordination between different branches of defense; the brakes the immune system puts on itself, so it does not put the hostâs own tissues at risk. Casanova and his colleagues are also on the hunt for mutations that might alter peopleâs risk of developing long COVID and other coronaviral consequences. None of these searches will be easy. But they should be at least simpler than the one for resistance to infection, Casanova told me, because the outcomes theyâre measuringâserious and chronic forms of diseaseâare that much more straightforward to detect.
If resistance doesnât pan out, that doesnât have to be a letdown. People donât need total blockades to triumph over microbesâjust a defense thatâs good enough. And the protection weâre born with isnât all the leverage weâve got. Unlike genetics, immunity can be easily built, modified, and strengthened over time, particularly with the aid of vaccines. Those DIY defenses are probably what kept Carringtonâs case of COVID down to âa mild course,â she told me. Immune protection is also a far surer bet than putting a wager on what we may or may not inherit at birth. Better to count on the protections we know we can cook up ourselves, now that the coronavirus is clearly with us for good.
This is my case, no doubt.
This most definitely is, too
Temperature was consistently above 99 until husband gets home and then we both go straight back to normal. COVID test I took was negative.
I donât understand what the universe is trying to tell me.
Yeah, Iâd be astonished if i were resistant. I catch colds. I think itâs just a combination of having been really careful and some good luck.
I think i probably am resistant to norovirus, though. Iâve been at two weekend events where everyone else caught it. And i ate from the same cookie jar they shoved their grimy hands into, shared m&ms from an open bag, shared pens and laptops⊠Both times everyone else had traditional norovirus symptoms, and i felt slightly under the weather.
But Iâm going to catch covid one of these days. And i doubt it will be the 3 days of sniffles version. 
There are lots of bugs other than covid that can give you a mild fever. You probably caught it at the same time and it ran its course on the same schedule.
Well, hopefully when you do it wonât even be that bad. I am not particularly healthy, get the flu and pneumonia on occasion, so perhaps I am similar to you to some degree, and I was almost asymptomatic.
Naw, Iâm terrified of covid. I get âlong coldsâ all the time. That is, it routinely took me longer than 2 weeks to recover from the common cold pre-covid. Ever since SARS COV 2 first hit the news, Iâve felt it has my name on it. A cold that can kill you is not my friend.
My husband, who rarely catches cold, actually had an asymptomatic case really early in the pandemic. (We only know because he gave platelets every two weeks, and the Red Cross was testing for it.) Iâm not especially worried about him, or my kids. And it already killed my mom. But Iâm really worried about it for me.
(also for my brother, who took so long to clear colds that he was seeing a pulmonologist about that when the pandemic hit.)
Of course, I had reasons to be afraid of the Shingles vaccine, and that was fine. I felt shitty for a day, and had a sort arm for a couple of days, and that was it.
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Just to add a data point, someone i know who similarly has a common cold lead to weeks of misery⊠when she caught covid, she took paxlovid and was over it in a few days. It ended up being a non event.
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GUYS, I just got back from the rheumatologist in my quest to check out every doctor that can possibly diagnose this fatigue Iâve had on and off.
ANYWAY, I just looked online and in my after visit summary, it SAYS THIS!
Temp:
37.3 °C (99.1 °F)
AM I READING THAT RIGHT? I COPY/PASTED IT. DOES IT SAY THAT IâM 0.5 DEGREES ABOVE NORMAL??? SHOULD I TAKE A COVID TEST ASAP! PLEASE LET ME KNOW! IâM FREAKING OUT YOU GUYS. KTHX.
If it were me Iâd want to know and would take one. 