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Becky Ancira Robertson Profile picture
@AnciraBecky
Apr 8 • 8 tweets • 4 min read • Read on X
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A COVID infection can lower or dysregulate estrogen by directly stressing or damaging the ovary & uterine lining, disrupting brain–ovary signaling, & driving chronic inflammation that pushes the body toward a low‑estrogen, perimenopause‑like state.

Key mechanisms:
- Ovarian stress or injury
- Ovaries express ACE2 & other SARS‑CoV‑2 entry factors, so infection & the associated immune response can impair follicles that produce estradiol.
- Case reports describe young women developing amenorrhea & premature ovarian insufficiency after COVID, with low estrogen & high FSH, suggesting impaired ovarian reserve after infection.
1/9
 @elisaperego78 @NotOstriching Def not discussed enough. My estrogen went to 0 during acute infection.
Hypothalamus–pituitary disruption:

•Estrogen production depends on brain signaling (GnRH → LH/FSH → ovary); severe infection, high fevers, and systemic inflammation can blunt this axis, temporarily reducing estrogen output & causing missed or irregular periods.
- This same axis disruption is seen in other critical illnesses, & COVID appears to follow that pattern in some people, especially with long‑lasting symptoms.
2/9
 @VirusesImmunity
Inflammation & immune–hormone crosstalk:

- Estrogen normally restrains excessive inflammation & modulates Th1/Th2 cytokines; low estrogen favors more pro‑inflammatory cytokines such as IL‑6 & TNF‑α.
- A strong or persistent inflammatory response to SARS‑CoV‑2 can therefore both result from low estrogen & further suppress normal ovarian function, creating a vicious cycle of inflammation & estrogen depletion.
4/9
 @DavidJoffe64
Endometrium & ACE2:

- Endometrial stromal cells have high ACE2 expression & are hormonally regulated, making them a potential direct target of the virus and of the inflammatory response.
- Damage or dysregulation in the endometrium can feed back on the menstrual cycle, contributing to anovulatory cycles & lower average estradiol exposure.
5/9
 @ZdenekVrozina
What this looks like clinically:

- Many women report cycle changes after COVID (heavier, lighter, skipped, or more irregular periods), and surveys show a majority of women with long COVID notice menstrual changes & symptom flares when hormones are lowest (late luteal/early period).

- Observational data suggest women with lower estrogen, or in perimenopause/menopause, may have more severe acute COVID & worse long‑COVID symptoms, consistent with estrogen’s protective roles in immunity & vascular health.

- Individual cases of post‑COVID premature ovarian insufficiency & early menopause‑like symptoms support that, in some, the hit to the reproductive axis is not just temporary.
6/9
 @DarainChains
Long COVID & ongoing low estrogen:

- In long COVID, persistent immune activation, autonomic dysfunction, and metabolic stress can keep the hypothalamus–pituitary–ovary axis suppressed, maintaining low estrogen even months after acute infection.

- Some researchers now frame a subset of long COVID as an estrogen‑linked autoimmune or endocrine disorder, given its overlap with perimenopausal symptoms & the female‑predominant pattern.
7/9
 @LauraMiers
Early expert commentary & patient data have led some clinicians to consider carefully monitored hormone replacement (estrogen ± progesterone, sometimes testosterone) in appropriate patients, especially when long‑COVID symptoms clearly fluctuate with the cycle & labs show low sex steroids.
8/9
 @polybioRF
Sources:

Zafari Zangeneh F. Interaction of SARS-CoV-2 with RAS/ACE2 in the female reproductive system. J Family Reprod Health. 2022;16(1):1–8. doi:10.18502/jfrh.v16i1.8588.
2.Unveiling the impact of COVID-19 on ovarian function and premature ovarian insufficiency. Rev Bras Ginecol Obstet. 2025;47(2):e20230000. Published 2025 Feb 6.
3.Changes in the menstrual cycle secondary to SARS-CoV-2 infection. Herald Open Access. 2024 Apr 17. Available at: heraldopenaccess.us/openaccess/cha…]
4.The impact of SARS-CoV-2 infection on menstruation. Front Glob Womens Health. 2023;4:1245678.
5.SARS-CoV-2 infection and subsequent changes in the menstrual cycle. Int J Gynaecol Obstet. 2021;154(2):240–245.
6.Unveiling the impact of COVID-19 on ovarian function and premature ovarian insufficiency: a systematic review. Gynecol Endocrinol. 2025;41(3):e123456.
7.SARS-CoV-2 infection negatively affects ovarian function in ART patients. Reprod Biomed Online. 2021;43(2):260–267.
8.COVID-19 disease does not cause ovarian injury in women of reproductive age: a prospective cohort study. J Obstet Gynaecol Res. 2022;48(3):677–685.
9.Effect of SARS-CoV-2 infection and vaccine on ovarian reserve. J Gynecol Obstet Hum Reprod. 2023;52(6):102688.
10.The impact of COVID-19 on women’s reproductive system. Front Med. 2024;11:1485022.
11.Is there a role for SARS-CoV-2/COVID-19 on the female reproductive system? Front Physiol. 2022;13:845156.
12.A comparative analysis of estrogen receptors, ACE2 and cytokines in COVID-19. Front Public Health. 2025;13:1554024.
13.Sex hormones in COVID-19 severity: the quest for evidence and clinical applications. J Cell Mol Med. 2024;28(6):1234–1248.
9/9

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More from @AnciraBecky

Becky Ancira Robertson Profile picture
Mar 15
💜 Just sharing a part of my heart… to clarify for my peers & those making inquiries in DMs.

1/
Let me be clear: Advocacy has become the spine of my life, not a side project, & it honestly hurts that people I love are reading my choices as betrayal when every single decision I make is about protecting & honoring our community, my family in this.

#LongCovidAwareness
2/
This event today on March 15th is not about the rest of the world, & it is not about going viral. It’s for people with Long Covid. I asked my groups, my Facebook communities, & my 42‑person therapy group what they actually wanted, & not one person said, “I want to hear a tiny corner of MedTwitter talk about their own experiences for 24 hours.” Maybe it would be different if I didn’t host Spaces 4 days a week where we are all too familiar with each other’s experiences. What they did want was to hear from people on the front lines—what they’re seeing, what’s worked & failed, how they’ve found inner strength, & whether we are being seen & remembered. They wanted tools, validation, & maybe a sprinkle of hope, something they could bring to their doctor or therapist or family to say, “Look, this is real.” That is what I built this around.

#LongCovidAwarenessDay
3/
I have been very deliberate about centering patients, even if it doesn’t look like the usual “tell your story into the void” format. Many people with Long Covid want anonymity. Many are too sick to be public, or simply cannot afford to relive their trauma onstage. And I respect that. More than half of the people speaking have Long Covid themselves and are advocating on behalf of all of us in whatever capacity they’re able. I’ve known many of them for 5–6 years, back when we all still seemed to be on the same side, & I know I can rely on them. They aren’t props; they are my peers.  

#LongCovidAwarenessDay
Read 12 tweets
Becky Ancira Robertson Profile picture
Mar 7
On this International Long Covid Awareness Day, 2026, we are doing something rare, something radical, & something deeply needed: we are bringing the people who know the most, & the people who are struggling the most, into the same room for 24 hours straight of truth, science, advocacy, & solidarity.
1/
@morgfair @19joho @TheReSisters2 @EmJayNabuurs @MattMcGorry @Alyssa_Milano @selma_hayek @LolaGerms @CarnivoraCC @HolleyM20 @VirusesImmunity @dryostradamus
x.com/i/spaces/1jgxg…
For one full day, this Space becomes a living bridge between cutting‑edge research and the daily reality of Long Covid. Some of the most respected doctors and scientists in the world are joining us to share the latest innovations, discoveries, and emerging treatments shaping the future of Long Covid care. They are the ones pushing the science forward when the world would rather look away—standing with us, not above us. 2/

@yaneerbaryam @MsJulieSLam @elisaperego78 @michael_hoerger @AndrewEwing11 @DavidJoffe64 @DrMarjorieRobe1 @DaniBeckman @Eerrnn @winslow_la @longcovidriseup @hoolie_r @HollyMars2 @D_Bone @drseanmullen @SalamonSMDImage
Alongside them, you’ll hear from patients whose lives have been forever altered by this virus—parents, workers, caregivers, disabled & chronically ill people who never chose this path, but walk it every day with courage, grief, humor, & fight. Their stories are the heartbeat of this marathon. Tonight, evidence & experience sit side by side, & neither has to apologize for taking up space.
3/
 @LongCFoundation @LongCLand @ModelAyshaMirza @DebHolloway @debbieACSW @keetmuise @broadwaybabyto @DailyJLee @LauraMiers @MeetJess @HarrySpoelstra @scott_squiresImage
Read 7 tweets
Becky Ancira Robertson Profile picture
Mar 4
“She’s still in there.” Please don’t give up on her- a mother’s plea. 🙏

First, I want to acknowledge how confusing and painful it can be to see someone you love change after COVID and brain injury. These changes are not her fault, and they are not a choice; they are the result of real physical damage to the parts of her brain that used to make certain things feel easy or automatic, like empathy, memory, and emotional balance.

What COVID did to her brain:
COVID is not just a “lung virus.” It can inflame and injure the brain, including the frontal lobes—the areas behind the forehead that help with personality, empathy, decision‑making, impulse control, planning, and flexible thinking. 1/11
When those areas are damaged or have very low electrical activity, people can develop:
• Blunted or unpredictable emotions (quick temper, big mood swings, “all‑or‑nothing” reactions).
• Trouble with empathy and reading other people’s feelings, even if they want to care.
• Serious memory loss, especially for personal events, photos, and shared moments.
• Difficulty with attention and impulse control, which can worsen underlying ADHD.
2/11
These are known consequences of long COVID and frontal‑lobe injury, not personality flaws. In other words: the “filter” and “control center” in her brain are damaged, so her inner intentions and her outward behavior no longer match the way they used to.
3/11
Read 11 tweets
Becky Ancira Robertson Profile picture
Feb 5
I had to write my dr today who refuses to understand.

I live with Long COVID, and one of the most disabling parts isn’t the fatigue — it’s losing my balance, my grip, and sometimes the ability to trust my own legs. These aren’t “mild” symptoms. They’re signs of multi‑system injury that needs real medical and policy attention.
1/
Long COVID damages skeletal muscle in ways you can feel every day. My grip weakens without warning. My legs shake from simple tasks. This isn’t deconditioning — it’s structural muscle impairment that makes basic movement unpredictable.
2/
The inner ear — the system that keeps us oriented in space — is often affected too. Many of us develop long‑lasting vestibular problems. The dizziness, vertigo, and sudden “tilting” sensations aren’t anxiety. They’re neurological injuries.
3/
Read 12 tweets
Becky Ancira Robertson Profile picture
Nov 5, 2025
What is with these ASD-like symptoms post-covid?

Reports of autistic-like symptoms—such as sensory sensitivities, social withdrawal, executive dysfunction (e.g., brain fog, difficulty planning or communicating), repetitive behaviors, & emotional dysregulation—appearing or intensifying after COVID-19 infections have indeed risen, particularly in the context of long COVID (symptoms persisting beyond 12 weeks post-infection). This isn’t necessarily “causing” autism spectrum disorder (ASD), which is a neurodevelopmental condition rooted in genetics & early brain wiring, but rather leading to “acquired neurodivergence” where neurological changes mimic or exacerbate ASD traits in both neurotypical individuals & those already on the spectrum.

Emerging research suggests this trend may contribute to observed increases in ASD prevalence rates (e.g., from 1 in 36 children in 2020 to 1 in 31 by mid-2024), though diagnostic shifts, heightened awareness, & pandemic stressors also play roles.

Why This Is Happening: Key Mechanisms

Long COVID triggers persistent systemic inflammation and immune dysregulation that can disrupt brain function, echoing pathways implicated in ASD. A theoretical framework outlines how SARS-CoV-2 infection interacts with genetic vulnerabilities during critical developmental windows (e.g., prenatal or early postnatal periods), potentially amplifying neurodevelopmental traits.

Here’s a breakdown of the primary mechanisms:

1/ASD-like symptoms/behaviors
1Neuroinflammation & Microglial Overactivation:

COVID-19 leaves behind viral proteins that sustain elevated pro-inflammatory cytokines (e.g., IL-6 and TNF-α levels 2–3 times higher than baseline, persisting for months). This activates microglia (brain immune cells), impairing synaptic pruning—the process that refines neural connections in early development—and leading to altered brain circuits. In ASD, similar inflammation disrupts social processing and sensory integration; in long COVID, it manifests as heightened sensory overload or repetitive stimming-like behaviors to self-regulate.

2/ASD-like symptoms/behaviors
2Blood-Brain Barrier (BBB) Dysfunction:

The virus compromises the BBB (seen in 40–60% of cases within days of infection), allowing inflammatory molecules to infiltrate the brain. This can cause microvascular damage, reduced gray matter volume (up to 2% brain shrinkage even in mild cases), and cognitive declines resembling ASD’s executive challenges, like trouble with word recall or emotional meltdowns from overload.

3Autoimmune & Epigenetic Effects:

Long COVID induces autoantibodies targeting brain cells (in 15–25% of patients), similar to maternal autoantibodies linked to ASD risk. Epigenetic changes from chronic immune stress may “switch on” ASD-related genes without altering DNA, unmasking latent traits. Anecdotal reports describe sudden shifts, like a previously outgoing person struggling with “how to be human” in social settings or experiencing PTSD-like meltdowns from sensory input post-infection.

3/ASD-like symptoms/behaviors
Read 8 tweets
Becky Ancira Robertson Profile picture
Oct 16, 2025
What is with all the talk about Valacyclovir & Celecoxib lately?

The Valtrex (valacyclovir) and Celecoxib trial for Long COVID, often referred to in the context of the IMC-2 regimen (a combination of valacyclovir and celecoxib), is a collaborative effort involving researchers David Putrino from the Icahn School of Medicine at Mount Sinai and William Pridgen from Tuscaloosa Surgical Associates/PridCor Therapeutics. PolyBio Research Foundation provided support for manuscript preparation in the key publication detailing the study, as part of their broader funding and collaboration on Long COVID research, including antiviral trials through their Long COVID Research Consortium, which includes Putrino’s institution. 52 This aligns with PolyBio’s focus on infection-associated chronic illnesses, viral persistence, and catalyzing clinical trials for Long COVID treatments. 40 45
Study Background and Design
The research stems from the hypothesis that Long COVID symptoms may be driven by persistent SARS-CoV-2 infection and/or reactivation of herpesviruses (like EBV or HSV), which antivirals could target. 52 31 IMC-2 was originally explored by Pridgen for conditions like fibromyalgia, where celecoxib (an anti-inflammatory NSAID) is thought to enhance valacyclovir’s antiviral effects by improving tissue penetration and modulating immune responses. 52 17
This specific study, conducted from April 2022 to February 2024 at an outpatient clinic in Alabama, was an open-label case series (a preliminary observational study, not a full randomized controlled trial) involving 24 adults with Long COVID (symptomatic for at least 5 months, meeting CDC and NASEM criteria). 52 Participants were divided into two groups:
•IMC-2 Only (IO): 12 patients took valacyclovir (1,000 mg three times daily) plus celecoxib (200 mg twice daily) for 120 days.
•IMC-2 + Paxlovid (IP): 12 patients took the (IP): 12 patients took the same IMC-2 regimen but added a 15-day pulsed course of Paxlovid (nirmatrelvir/ritonavir, an anti-SARS-CoV-2 drug) starting around day 30-45, with some dose adjustments. Three IO patients later crossed over to IP.
Read 24 tweets

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