Thread by @ZdenekVrozina

This new Nature Communications study is the most comprehensive look we’ve ever had at SARS-CoV-2 inside the human fetus.
And the message is straightforward.
Vertical transmission is real,
and the virus can reach multiple fetal organs - even early in pregnancy🧵

For years we heard that fetal infection was rare.
But that was based on limited testing, often using low-sensitivity methods.

When you apply ddPCR, subgenomic RNA, RNAscope, immunofluorescence and TEM, a different picture appears.
The virus can infect the fetus - and more often than previously recognized.

The study found that 10% of all fetal samples were SARS-CoV-2 positive. In some fetuses, the virus appeared in multiple organs at once. 21 tissues carried a high viral load, and 10 showed active viral replication.

The organs most affected were
thymus (where T cells develop)
thyroid gland (crucial for brain development)
digestive tract
kidneys
and testes.
These are precisely the organs undergoing rapid development in early gestation.

The thymus is the standout.
It showed some of the highest viral loads and clear inflammatory activation (HMGB1, CD11B, CD86).
That matters.

It means SARS-CoV-2 can disturb T-cell development before birth - potentially shaping how the child’s immune system works later in life.

The thyroid gland was another high-burden organ.
And since thyroid hormones guide fetal brain development, inflammation or injury here could influence neurodevelopment - even if the virus barely enters the brain itself.
This is an indirect but biologically plausible pathway.

The study also shows that fetal tissues express ACE2 and TMPRSS2, the same proteins the virus uses to enter cells in adults. So no - the fetus isn’t protected because it lacks the receptor.
The molecular doorway is there, even early on.

One of the most important findings is a strong suppression of DNA repair pathways in infected organs.
This aligns with what we know. The N protein of SARS-CoV-2 interferes with DNA damage responses.
During fetal development - when cells are dividing rapidly - this is a serious biological stressor.

In infected organs the team saw
signs of tissue injury, activation of pro-inflammatory macrophages, and increased fibronectin (marker of fibrosis).
This is the same pathological signature we see in adult COVID - just in much more sensitive tissue.

Only two placentas tested positive for viral RNA, but many fetuses were infected.
This likely means that infection is patchy, or occurs through small, localized breaches or through the membranes - not always in the sampled placental area.

So a negative placenta does not guarantee the fetus was protected.

Timing mattered.
The shorter the interval between maternal infection and pregnancy termination, the more viral-positive organs the fetus had.
Early pregnancy - when organs are forming - is clearly the most vulnerable window.

Put together, this study provides strong evidence that SARS-CoV-2 is a true fetal pathogen.

It doesn’t just cross into the fetus - it alters tissues, suppresses DNA repair, triggers inflammation, and targets organs essential for immunity and neurodevelopment.

If the virus disrupts the thymus or thyroid during critical developmental windows, the consequences may not show up at birth - but later, during childhood.
Long-term follow-up will be essential.

Wu at al., Presence of SARS-CoV-2 in fetal organs via intraamniotic infection.
Nature Communications 2025. nature.com/articles/s4146…

The risks were known as early as 2020-2021. Even as more studies emerged showing placental damage, and risks for newborns, public health authorities never bothered to systematically warn pregnant women.

This new study only confirms it: the risk was there all along - and it was ignored.
@szupraha @ZdravkoOnline @adamvojtech86

The result? Parents are left in the dark. And pregnant women - one of the most vulnerable groups - ended up being paradoxically the least protected. They should have received the clearest, earliest and most transparent information.