cynthia mahoney ❌👑

Long Covid & Viral Persistence - The splinter is real. Now let’s figure out how to remove it. This analogy recently came to mind. Probably about 30 years ago, I had a teacher use the following example, of a rock in your shoe. She said, "You can ignore it, try to walk it off. Try to be a tough guy. Just try to get over it. Or you can take off your shoe and remove the rock." We need to start thinking in practical ways. I’ve adapted this to the current science. A splinter makes the example more relevant, as it feels like something much more stuck. The Splinter - Viral Persistence? If you have a splinter in your finger, you can put bandages on it, take pain medication, and learn to live with the discomfort. But the real solution is to find the splinter and remove it. I know many have been waiting for answers. Been told to rest, or to try harder. You’ve seen doctors who don’t know how to help. Family dismisses you when medicine has no answers, and they are left wondering if you’re losing your mind. But here’s what science is starting to find, and it’s not what many expected in 2020. The virus didn’t leave your body the way it was supposed to. This isn’t about you being weak or a flawed person. This is about a virus that has evolved sophisticated ways to hide in your tissues, continuing to cause havoc long after everyone thought you should be “recovered.” It’s actually not uncommon. Lots of viruses stick around and go dormant. Remember chickenpox, mono, hepatitis? Some are suppressed with drugs to keep them down like HIV. The list is actually quite long. What We Mean When We Say “Persistence” When scientists talk about viral persistence, they’re describing something very specific: the virus or its components staying in your body well beyond the acute infection phase. This isn’t just leftover debris, though that’s part of the story too. Think of it like this: imagine someone broke into your house, trashed the place, and left. The obvious damage you can see and repair. But what if they also planted tiny devices throughout your home that kept malfunctioning your electrical system, your plumbing, your heating? That’s more like what SARS-CoV-2 persistence looks like. We measure this in several ways, and not all evidence carries the same weight. Finding viral RNA or proteins in your blood or tissues months after infection is suggestive, but it could just be leftover fragment, the equivalent of finding broken glass weeks after a burglary. What’s more convincing is when we find molecular signatures that the virus is still actively replicating: double-stranded RNA, antisense RNA, or subgenomic RNA. These are like finding fresh footprints or hearing the burglar still moving around upstairs. The strongest evidence? When we can track how the virus evolves within a single person over time. Evolution requires replication, and replication means the virus is still alive and active in your body. The Growing Mountain of Evidence The research has been building steadily, and it’s painting a picture that many of us didn’t want to believe. Multiple autopsy studies have found viral RNA and proteins scattered across organs—brain, gut, heart, kidneys, months after people died from other causes. These weren’t people who died from acute COVID; these were people who had “recovered.” In living people, gut biopsies tell an even more compelling story. Researchers have found not just single-stranded viral RNA (which could be debris), but double-stranded spike RNA in tissue samples taken up to 670 days—nearly two years—after symptom onset. Double-stranded RNA argues for ongoing transcription. The virus isn’t just sitting there dead; it’s actively making copies of itself. A major study published in The Lancet Infectious Diseases sampled multiple tissues from people who’d had mild COVID infections and directly linked the presence of tissue RNA with symptoms that persisted after “recovery.” The virus was there, and where it was hiding correlated with what people were experiencing. Blood tests using ultra-sensitive assays can now detect viral spike protein or nucleocapsid months after infection. People with Long COVID are about twice as likely to have these viral proteins circulating in their blood compared to those without persistent symptoms. This isn’t subtle, it’s a clear signal that something is still there, still active. Teams at UCSF and other major institutions have reported finding viral RNA in blood through 14 months and in connective tissue beyond two years. These findings were presented at major infectious disease conferences with full institutional backing. This isn’t fringe science anymore. What Hasn’t Been Settled Yet The one piece that keeps some scientists cautious is that culturing live, infectious virus from Long COVID patients remains difficult and uncommon. Some studies can grow virus during acute disease but can’t recover live virus months later from the same people. This technical gap is why some researchers remain skeptical, even as the molecular evidence accumulates. But here’s the thing about viral culture: it’s finicky under the best circumstances. Low-level replication, tissue access limitations, and sample handling issues all make culture challenging. The absence of culturable virus doesn’t mean the virus isn’t there, it might just mean we haven’t figured out how to grow it in the lab yet. We also can’t just cut into people for the sake of a study. Meanwhile, multiple studies are connecting persistence signals with symptoms over time. People with documented viral persistence have higher odds of reporting Long COVID symptoms at 12 weeks and beyond. The pattern is consistent across different research groups and different types of testing. Why This Isn’t the Only Story Long COVID is almost certainly not just one thing. It’s probably several different disease processes that can overlap and interact. Viral persistence appears to be one important mechanism, but it’s not the whole story. We have solid evidence for immune system dysfunction and autoimmunity. Researchers have transferred antibodies from Long COVID patients to mice and reproduced some of the symptoms. Reviews are documenting how B cells and autoantibodies might be driving ongoing problems. Reactivation of latent viruses like Epstein-Barr appears in multiple studies. When your immune system is dysregulated from fighting persistent SARS-CoV-2, other viruses that have been quietly sleeping in your body can wake up and cause additional havoc. Microclots and blood vessel dysfunction are now well-established features of Long COVID. These aren’t the large clots that cause heart attacks or strokes, they’re microscopic, abnormal protein deposits that resist the body’s normal clot-dissolving mechanisms. Multiple independent research groups have documented these fibrinaloid microclots in Long COVID patients using specialized fluorescent staining techniques. The microclots block tiny capillaries, reducing oxygen delivery to tissues throughout the body. When Long COVID patients exercise, these clots can fragment into smaller pieces, causing additional vascular injury and explaining why physical activity often worsens symptoms for days or weeks afterward. This vascular pathology helps explain the wide range of Long COVID symptoms, when oxygen delivery is compromised at the cellular level, every organ system can be affected. The smart approach isn’t to pick one mechanism and ignore the others. It’s to study them all and understand how they might work together or affect different people in different ways. What the Treatment Trials Are Teaching Us This is where it gets both hopeful and frustrating. If viral persistence is driving Long COVID in some people, then antiviral medications should help those people. The trials are starting to give us answers, but they’re revealing important limitations in our current approach. The Antiviral Challenge A randomized trial of nirmatrelvir-ritonavir (Paxlovid) in people with established Long COVID was safe but didn’t improve symptoms in the overall group. However, this result isn’t particularly surprising when you understand viral persistence better. Paxlovid was designed for acute COVID treatment, a 5-day course to prevent severe illness. But persistent SARS-CoV-2 appears to hide in immune-privileged sites where drug penetration is limited and where viral replication may be slow and intermittent. Think about what we know from HIV treatment. It took years to understand that HIV could establish latent reservoirs in tissues where standard drug regimens couldn’t reach effectively. Even with highly effective antiretroviral therapy, it can take months to see full effects on tissue viral loads, and some reservoirs persist indefinitely. SARS-CoV-2 persistence likely operates similarly. The virus appears to establish reservoirs in gut tissue, lymph nodes, and possibly other sanctuary sites where immune surveillance is reduced and drug access is limited. A 5-day or even 15-day course of an antiviral designed for acute treatment may be inadequate to clear established reservoirs. Other countries are taking different approaches. China has developed several COVID-19 antivirals with different mechanisms of action and tissue distribution profiles. Azvudine, approved in China and some other countries, was originally developed as an HIV drug and may have better tissue penetration. VV116 (leritrelvir) showed promise in Chinese trials and has different pharmacological properties than Paxlovid. The lesson from early antiviral trials isn’t that viral persistence can’t be treated—it’s that we need longer treatment durations, better tissue-penetrating drugs, and probably combination approaches. Case reports of extended antiviral courses (30-90 days) in carefully selected patients show more promising results, though these need rigorous controlled validation. The Promise of Monoclonal Antibodies Here’s where things get really interesting. Some Long COVID patients have experienced remarkable recoveries after receiving monoclonal antibody treatments, even when those treatments were given months or years after their original infection. The most compelling evidence comes from case reports published in The American Journal of Emergency Medicine in 2023. Three previously healthy, middle-aged people with severe, debilitating Long COVID received monoclonal antibody infusions for unrelated reasons, either to treat a second COVID infection or prevent illness after an exposure. What happened next was extraordinary: each person experienced complete remission of their Long COVID symptoms within days of the infusion. These weren’t subtle improvements. These were people who had been severely disabled for months, suddenly returning to full function and vitality. Two or more years later, they remained healthy and symptom-free. The recoveries occurred despite differences in age, sex, medical history, vaccination status, and how long they’d had Long COVID. The theory is that monoclonal antibodies can bind to and clear persistent viral antigens that are continuing to trigger immune activation and inflammation. Unlike antivirals that need to penetrate tissues and stop active replication, antibodies work by neutralizing viral proteins wherever they encounter them in the body. However, rigorous testing has been more complicated. A recent placebo-controlled trial at UCSF found that monoclonal antibodies didn’t provide universal benefit for Long COVID patients. Some people in both the treatment and placebo groups improved, while others saw no change. The researchers weren’t discouraged, though, they learned important lessons about patient selection and treatment timing. The key insight is that monoclonal antibodies probably won’t help everyone with Long COVID, but they might be transformative for specific subgroups. The challenge is identifying which patients are most likely to benefit, probably those with detectable viral antigens or specific immune signatures that suggest ongoing viral persistence. Future trials should focus on biomarker-positive patients treated with antibodies specific to their original infecting variant, potentially with combination regimens designed to address tissue reservoirs rather than just circulating antigens. What This Means for Your Daily Life If you’re living with Long COVID, this research validates what you’ve been experiencing. Your symptoms aren’t “all in your head,” and you’re not just being dramatic. There are measurable, biological processes happening in your body that explain why you feel the way you do. This also means that treatments targeting viral persistence might help some people. We’re not there yet with proven therapies, but the research direction is promising. Clinical trials are ongoing, and more are being planned. For families trying to understand: your loved one isn’t choosing to be sick. They’re not exaggerating or avoiding responsibility. Their body is fighting an ongoing infection that standard medical tests often can’t detect. The fact that they look fine from the outside doesn’t change what’s happening on the inside. Where We Go From Here The research community is converging on some clear priorities. We need paired tissue and blood studies in living people, using standardized protocols that different labs can reproduce. We need focused clinical trials on viral persistence! With millions of Americans, no experiencing on Covid, this is critical. We need to map exactly where the virus is hiding and how it’s affecting different organ systems. A Personal Note I want to be clear about something: this research doesn’t guarantee that everyone with Long COVID has persistent virus, or that antivirals or monoclonal antibodies will cure everyone who tries them. Science is messy and slow, and individual biology is complicated. But what this research does provide is biological validation for experiences that have been dismissed and minimized. It offers rational explanations for symptoms that seemed inexplicable. And it points toward treatment strategies that target base causes rather than just managing symptoms. For those of you who have been fighting to be believed, to be taken seriously, to be treated as more than psychiatric cases: the evidence is mounting in your favor. Science is catching up to your lived experience. For families and friends who have struggled to understand: your loved one’s illness has biological basis. Their limitations are real. Their suffering deserves the same compassion and support you would give anyone with a serious medical condition. We’re not at the finish line yet, but hopefully it’s going to be forced into the light, and that’s the first step toward showing it the door. The splinter is real. Now let’s figure out how to remove it!

I see a ton about long covid from legitimate, scientific sources that if it was even remotely true would have apocalyptic implications, everyone’s heart, lungs, and brain failing at once, and I can’t square it with the world I actually observe every day.

This captain in the National Guard has an urgent warning for National Guardsmen who are being deployed and used as Gestapo pawns in the authoritarian dictator-wannabe's fascist power grab. 😳👇

When this constituent asks GOP Rep. Mike Flood is he'd support Medicare For All, the Congressman says "We can't afford that." The crowd at the town hall immediately starts booing.

Don’t F*ck with Moms. I was raised by a single mom as an only child just outside Washington DC. She worked for the federal government that is currently being dismantled, and when she got cancer, it was her government insurance and pension that gave her five more years with her grandkids. The adventure of trying to save her life through the medical system was both an indictment of profit-motivated health care, and a shining example of the government taking care of its own. The treatment we were finally able to find her gave her those extra years, but it would have been impossible if she hadn’t been a former government employee.  Needless to say, the current regime is destroying all those bonds, that trust, is trying to destroy the government’s role in health care for everyone, and is attacking the rights of all women, not just moms. In my work over the last five years, I’ve met thousands of people but of the small core group that I work with, that I have grown to trust with my own life, most of them are moms. This is not an accident, or just a function of my own background. Mothers are fiercely protective, deeply connected to the real world, and by definition are able to give without expectation of immediate return. In an environment where information and trust are everything, those are the people that I rely on, who have lifted me up, and helped me survive some very hard times. To destroy a society, or to control it, the easiest way to divide and conquer is to split men and women apart. Misogyny has been a tool of despots, dictators and cult leaders since the dawn of civilization, and the current lurch in their direction is no exception. Putin, Orban and Erdogan have established misogyny as law which is the direction the current American regime is headed. Trump, JD Vance, Musk, Thiel and Flynn, just as examples, are all committed male supremacists who think women should be forced to have babies and be systematically repressed by the state. This revanchist, patriarchal attitude is, needlessly to say, backed up by the religious cult that has captured the U.S. Supreme Court. Well, on this Mother’s Day, I’m here to tell you, as much as moms are inherently giving, they are also built to fight when threatened. The war on women is a war that men will lose. My love and respect to GalSquad, Heidi, Jackie, and all the other mother warriors I have been honored to meet on this journey. Happy Mother’s Day to all. Don’t fuck with moms. 💙