As a frequent target of harassment who routinely receives threats of physical & sexual violence, Dr. Gottlieb nails it.
I cope because it's valuable to advocate for scientists & public health as best I can & I'm fortunate to have this platform. But Twitter can do better.
And I'm not the only one. Many of my colleagues have had similar run-ins with people threatening us, our friends, & our families. And accounts that consistently encourage this behavior continue unchecked, as do those that actually engage in this behavior.
Here's an example. This account has been locked multiple times for violations of every @TwitterSafety rule in the book, yet is still not suspended. "Violent threats," "Hateful conduct," "Abusive behavior"...still gets his nth 2nd chance to regain access.
Here's one tweet that I reported from this account. I tagged @TwitterSafety. Nothing happened. Meanwhile he was free to harass me & numerous colleagues ad nauseum. And several bigger, verified accounts kept following him, winking at him & amplifying him.
And what was amplified? Sharing personal information about people's family members, including their children. Naming their workplaces & schools. Encouraging people to harass them there. False allegations of serious crimes. Abhorrent sexism, racism, & ableism. Viciousness. Lies.
Only after weeks of this did @TwitterSafety step in. But vast damage can be done in that time. Not only does this encourage people to harm others, it can encourage the targets to harm themselves. So miss me with "but we can't censor people or silence the debate" excuses.
A relentless campaign of social media abuse can inflict severe damage to the target's mental health. That's the point: to break down the target by causing them so much anguish and endangering them to the point they leave the debate.
So who exactly is being silenced here?
Being the subject of a Twitter brigade can be agonizing. It's doubly so when you talk about what has happened to you & the pain it has caused, & that's trivialized & you are blamed for bringing it upon yourself.
This is not about disagreement or insulting people. It's a tactic.
And @TwitterSafety needs to seriously improve its ability to distinguish between protected speech—even when it's offensive—and patterns of dehumanizing abuse before they get to the stage of causing irreparable physical or emotional harm.
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Out now on @virological_org: preliminary report on the genomic epidemiology of H5N1 sequences in cattle. This complements the preprint @USDA put out yesterday.
There was a lot of data to work with, so it's split in two parts 👇🏼
1. There was a reassortment event shortly before the cattle outbreak.
Only segmented viruses like influenza can reassort. If 2 viruses infect the same host, they can shuffle their genome segments like 2 decks of cards
1. Reassortant viruses can acquire new features, including the ability to replicate efficiently in new host species. In this case, some of the segments were from the high path Eurasian panzootic H5N1 genotypes & some from low path North American genotypes emerging in late 2023.
Very important to note here that qPCR positives are not the same as "virus particles." It's much easier to detect viral RNA by qPCR than it is to detect infectious virus or intact virus particles (as the article correctly notes).
1. This suggests there are undetected herds shedding virus into the milk supply. Viral RNA does not materialize out of thin air—it is the product of a current or very recent viral infection.
No virus replicating in cows, no viral RNA in milk.
No viral RNA, no PCR positives.
1+. qPCR detects virus by amplifying small specific fragments of the viral genome. There's no indication that they pulled entire H5N1 genome sequences out of this, which would likely require signaling. Influenza is segmented, however, so no word on which segments they amplified.
Here is the article linked above and what it actually says: “The Texas Animal Health Commission said in an email that sick cats tested positive for the virus.”
There may be more cats affected but I did not find a single credible report of more than these 3 cats (for now). Also to be clear there is no evidence that it is “spreading rapidly” in mammals & sequence data suggests transmission from birds.
The only things created or crafted here are these grossly incorrect heaps of horseshit generated by @caitlintilley @DailyMail & @nypost.
This article and others like it are very misleading. This was not gain-of-function research, no matter how many loud non-experts say it is.
This article describes this recent preprint published on @biorxivpreprint. Briefly, scientists in Beijing cloned a pangolin SARS-related coronavirus they had isolated & infected human ACE2 transgenic mice with it. All the mice died.
Mice have ACE2 (the receptor that many SARSr-CoVs use to enter a cell) but it’s not similar enough to human to allow efficient entry of SARSr-CoVs that infect humans. So to study these viruses in mice, you need mice that express a human ACE2 transgene.
In this commentary, me and 77 of my colleagues argued that virology research is essential to pandemic preparedness. Biosafety is a cornerstone of virology research, but technical expertise is required for regulation that actually works & can’t be excluded from policy development.
All of the co-authors are US-funded virologists like me, who have technical expertise in experimental virology or vaccinology, or biosecurity and biosafety policy experts who agree that technical expertise is required to implement effective oversight.
This recent paper in @ScienceTM has a few of my favorite things:
✔️host-targeting drugs
✔️promising broad-spectrum antivirals
✔️international collaboration
It also demonstrates why continued virus discovery & virology research are critically important. science.org/doi/10.1126/sc…
Led by researchers at @harvardmed, @WuHanUniv, & @IcahnMountSinai, Dang, Bai, Dong, Hu, and colleagues targeted a protein called USP2, a deubiquitinase that stabilizes ACE2.
ACE2 is the receptor that allows SARS-CoV-2 and other SARSr-CoVs to enter cells and cause infection.
How does USP2 stabilize ACE2?
One way cells regulate protein expression is by tagging them with a little protein called ubiquitin, which means “degrade me”.
Not in the figurative sense, but in the sense of “take me to the proteasome and chop me up.”