Happy 2021! @MBVanElzakker and I are excited to share our new article published in #Immunometabolism: “Pathogens Hijack Host Cell Metabolism: Intracellular Infection as a Driver of the Warburg Effect in Cancer and Other Chronic Inflammatory Conditions”:

2/ In the paper, we detail molecular mechanisms by which #viral, #bacterial, and #parasite intracellular pathogens can induce, or contribute to, a Warburg-like #metabolism in infected host cells in order to meet their own replication and nutritional needs.
3/ We also discuss how host defense towards #infection may impact cellular metabolic changes (including how #mitochondria can participate in the innate immune response towards infection)
4/ We then provide examples of how many of these same intracellular pathogens have been identified in #tumors, atherosclerotic lesions, #granuloma, and other tissues containing cells with a Warburg or altered metabolism.
5/ Last, we examine further trends associated with infection and host cell metabolism, including how #pathogen-driven hijacking of host cell lipid metabolism can support viral, bacterial, and parasite survival and replication.
6/ Overall we argue that, at least in a subset of patients w/ #cancer, #atherosclerosis, #sarcoidosis + related conditions, metabolic changes and inflammatory cascades central to the disease process are driven by intracellular pathogens
7/ We also discuss how pathogen-driven hijacking of cellular metabolism may contribute to #MECFS. ME/CFS is an extremely debilitating #neuroinflammatory condition that often begins with an infection (w/ #herpesvirus or enterovirus involvement already documented in some cases)
8/ A better understanding + acceptance of the trend could result in novel #diagnostics and treatments for patients w/ such conditions (w/ discussion of how a #ketogenic diet might impede pathogen-hijacking of host metabolism)
9/ So many cool people helped make the paper a reality. Special thanks to @lenapernas @Palmer_IMet_lab @dbkell, Dr. Wonder Drake, and @krisfobes for helping us with feedback and on earlier drafts of the manuscript.

More from Science

https://t.co/hXlo8qgkD0
Look like that they got a classical case of PCR Cross-Contamination.
They had 2 fabricated samples (SRX9714436 and SRX9714921) on the same PCR run. Alongside with Lung07. They did not perform metagenomic sequencing on the “feces” and they did not get


A positive oral or anal swab from anywhere in their sampling. Feces came from anus and if these were positive the anal swabs must also be positive. Clearly it got there after the NA have been extracted and were from the very low-level degraded RNA which were mutagenized from

The Taq.
https://t.co/yKXCgiT29w to see SRX9714921 and SRX9714436.
Human+Mouse in the positive SRA, human in both of them. Seeing human+mouse in identical proportions across 3 different sequencers (PRJNA573298, A22, SEX9714436) are pretty straight indication that the originals

Were already contaminated with Human and mouse from the very beginning, and that this contamination is due to dishonesty in the sample handling process which prescribe a spiking of samples in ACE2-HEK293T/A549, VERO E6 and Human lung xenograft mouse.

The “lineages” they claimed to have found aren’t mutational lineages at all—all the mutations they see on these sequences were unique to that specific sequence, and are the result of RNA degradation and from the Taq polymerase errors accumulated from the nested PCR process
JUST ONE PERSON—UK 🇬🇧 scientists think one immunocompromised person who cleared virus slowly & only partially wiped out an infection, leaving behind genetically-hardier viruses that rebound & learn how to survive better. That’s likely how #B117 started. 🧵 https://t.co/bMMjM8Hiuz


2) The leading hypothesis is that the new variant evolved within just one person, chronically infected with the virus for so long it was able to evolve into a new, more infectious form.

same thing happened in Boston in another immunocompromised person that was sick for 155 days.

3) What happened in Boston with one 45 year old man who was highly infectious for 155 days straight before he died... is exactly what scientists think happened in Kent, England that gave rise to #B117.


4) Doctors were shocked to find virus has evolved many different forms inside of this one immunocompromised man. 20 new mutations in one virus, akin to the #B117. This is possibly how #B1351 in South Africa 🇿🇦 and #P1 in Brazil 🇧🇷 also evolved.


5) “On its own, the appearance of a new variant in genomic databases doesn’t tell us much. “That’s just one genome amongst thousands every week. It wouldn’t necessarily stick out,” says Oliver Pybus, a professor of evolution and infectious disease at Oxford.

You May Also Like