“Vaccines, obviously, are the ultimate solution for pandemics,” Rino Rappuoli told BioWorld. They have, he added, “already eliminated a lot of pandemic threats – smallpox, influenza, poliomyelitis.” And the road to normalcy from the current pandemic, or any pandemic, is likely to be open only once there is a vaccine.

Specific therapies against a new disease take time to develop. But there are methods that can speed up that development – and in the meantime, there are ways to make do with what’s already in the cupboard.

There will be lessons learned aplenty when the COVID-19 pandemic finally breaks, including how serological and molecular testing can be used to maximum effect to corral a future pandemic. Carmen Wiley, president of the American Association of Clinical Chemistry, told BioWorld that the existing instrument types are up to the job, but that surge capacity is needed, and that it is not clear how the cost of that capacity will be handled.

“In any crisis, leaders have two equally important responsibilities: solve the immediate problem and keep it from happening again... The first point is more pressing, but the second has crucial long-term consequences.” So wrote Bill Gates in a February editorial in The New England Journal of Medicine about COVID-19, which “has started behaving a lot like the once-in-a-century pathogen we’ve been worried about.”

BioWorld looks at translational medicine, including: Microbiome changes precede tumor development in CRC; Converting catch and release to PARP traps; Smart bacterium senses environment; The dose makes the poison – timing, too; Minimal phenotyping gives minimal insights into MDD genetics; Hypoxia linked to common form of muscular dystrophy; Stopping tau in its tracks; Optogenetic plaque model traces neurodegeneration in AD; Once repulsive, always repulsive.

COVID-19 has disrupted science in the way it has disrupted everything else. In the short term, universities have largely closed shop as a way to maximize social distancing, and lots of science – or at least, lots of bench work – is not getting done.

Indian scientists have discovered a previously unknown mechanism underlying life-threatening sepsis and proposed a new treatment strategy centered upon cell-free chromatin (cfCh), they reported in the March 4, 2020, edition of PLOS ONE. Notably, they showed that sepsis could be caused by cfCh released from dying host cells following microbial infection.

LONDON – Two papers published online in Nature following accelerated peer review provide fine detail of how the spike protein on the COVID-19 coronavirus binds to the angiotensin converting enzyme 2 (ACE2) through which it infects its human host.

As organisms adapt to their environment, adaptations that serve them in their current environment can become liabilities if that environment changes. The control of traits that are an asset in one situation and a liability by the same gene is called antagonistic pleiotropy. In the March 16, 2020, online issue of Nature Genetics, researchers reported a method to systematically identify mutations that conferred antagonistic pleiotropy – in the form of resistance to one drug, but heightened sensitivity to another – in acute myeloid leukemia (AML) cells.

BioWorld looks at translational medicine, including: How the eye cleans itself up; In blood stem cells, selection drives driver mutations early on; Dead cells do tell tales; Selective TGF-beta inhibition helps checkpoint blockade; How lung tumors seed to brain; Butyrate affects regulatory B cells, rheumatoid arthritis; Lamin A/C’s presence in nucleus, absence from membrane both problematic in progeria; Females, males have different metabolic response to intermittent fasting; Ditching PAMs expands CRISPR.