Infectious disease

Alexsia Richards is a postdoc in Whitehead Institute Member Rudolf Jaenisch’s lab investigating how dangerous tropical viruses interact with the brain. We sat down with Richards to learn more about her and her experiences in and out of the lab.

Boryana Petrova is a postdoc in Whitehead Institute Member Sebastian Lourido’s lab researching parasite metabolism. She has also worked in Whitehead Institute Member Terry Orr-Weaver’s lab. We sat down with her to learn a bit more about her and her experiences in the lab.

By identifying new compounds that selectively block mitochondrial respiration in pathogenic fungi, Whitehead Institute scientists have identified a potential antifungal mechanism that could enable combination therapy with fluconazole, one of today’s most commonly prescribed fungal infection treatments. Severe, invasive fungal infections have a mortality rate of 30-50% and cause an estimated 1.5 million deaths worldwide annually. Current antifungal therapies are hampered by the increasingly frequent emergence of drug resistance and negative interactions that often preclude combination use.

The germinal centers that form in the body’s lymph nodes work as a fitness boot camp in which B cells evolve to produce antibodies of increasingly higher affinity to an invading pathogen. This new finding from Whitehead Institute scientists overturns a previously held notion that only a narrow range of B cells can survive this training and go on to secrete high-affinity antibodies. This revised understanding may aid development of effective vaccines against HIV, influenza, and other viruses that mutate rapidly.

The most common fungal pathogen in humans, Candida albicans, rarely develops resistance to the antifungal drug amphotericin B (AmB).  This has been puzzling as the drug has been in clinical use for over 50 years. Whitehead Institute scientists have now discovered why.  The genetic mutations that enable certain strains of C. albicans to resist AmB simultaneously render it highly susceptible to environmental stressors and disarm its virulence factors.