It’s an inescapable conclusion from the book of Ecclesiastes that’s become part of popular culture thanks to folk legends Pete Seeger and The Byrds: “To everything (turn, turn, turn), there is a season.” That’s certainly true of viral outbreaks, from the flu-causing influenza virus peaking each year in the winter to polio outbreaks often rising in the summer. What fascinates Micaela Martinez is, while those seasonal patterns of infection have been recognized for decades, nobody really knows why they occur.
Martinez, an infectious disease ecologist at Princeton University, Princeton, NJ, thinks colder weather conditions and the tendency for humans to stay together indoors in winter surely play a role. But she also thinks an important part of the answer might be found in a place most hadn’t thought to look: seasonal changes in the human immune system. Martinez recently received an NIH Director’s 2016 Early Independence Award to explore fluctuations in the body’s biological rhythms over the course of the year and their potential influence on our health.
Caption: Birth years of people in China who contracted H7N9 avian flu from 1997-2015 (left); birth years of people in Cambodia, China, Egypt, Indonesia, Thailand, and Vietnam who contracted H5N1 avian flu from 1997-2015 (right). Source: Adapted from Science. 2016 Nov 11;354(6313):722-726.
You probably can’t remember the first time you came down with the flu as a kid. But new evidence indicates that the human immune system never forgets its first encounters with an influenza virus, possibly even using that immunological “memory” to protect against future infections by novel strains of avian influenza, or bird flu.
In a study that looked at cases of bird flu in six countries in Asia and the Middle East between 1997 and 2015, an NIH-supported research team found that people born before 1968 were at lower risk of becoming seriously ill or dying from the H5N1 strain of the bird flu virus than were those born afterwards . Just the opposite was true of another emerging strain of bird flu. People born before 1968 were at greater risk of becoming seriously ill or dying of H7N9, while those born after that date were more often protected.
Caption: An NCATS researcher dispenses Zika virus into trays for compound screening in a lab using procedures that follow strict biosafety standards. Credit: National Center for Advancing Translational Sciences, NIH
In response to the health threat posed by the recent outbreak of Zika virus in Latin America and its recent spread to Puerto Rico and Florida, researchers have been working at a furious pace to learn more about the mosquito-borne virus. Considerable progress has been made in understanding how Zika might cause babies to be born with unusually small heads and other abnormalities and in developing vaccines that may guard against Zika infection.
Still, there remains an urgent need to find drugs that can be used to treat people already infected with the Zika virus. A team that includes scientists at NIH’s National Center for Advancing Translational Sciences (NCATS) now has some encouraging news on this front. By testing 6,000 FDA-approved drugs and experimental chemical compounds on Zika-infected human cells in the lab, they’ve shown that some existing drugs might be repurposed to fight Zika infection and prevent the virus from harming the developing brain . While additional research is needed, the new findings suggest it may be possible to speed development and approval of new treatments for Zika infection.
Caption: eOD-GT8 60mer nanoparticle based on the engineered protein eOD-GT8. Yellow shows where eOD-GT8 binds antibodies; white is the protein surface outside the binding site; light blue indicates the sugars attached to the protein; dark blue is the nanoparticle core to which eOD-GT8 has been fused. Credit: Sergey Menis and William Schief, The Scripps Research Institute
A while ago, I highlighted a promising new approach for designing a vaccine against the human immunodeficiency virus (HIV), the cause of AIDS. This strategy would “take the immune system to school” and teach it a series of lessons using several vaccine injections—each consisting of a different HIV proteins designed to push the immune system, step by step, toward the production of protective antibodies capable of fending off virtually all HIV strains. But a big unanswered question was whether most people actually possess the specific type of precursor immune cells that that can be taught to produce antibodies that kill HIV.
Now, we may have the answer . In a study published in the journal Science, a research team, partly supported by NIH, found that the majority of people do indeed have these precursor cells. While the total number of these cells in each person may be low, this may be all that’s needed for the immune system to recognize a vaccine. Based in part on these findings, researchers plan to launch a Phase 1 clinical trial in human volunteers to see if their latest engineered protein can find these precursor cells and begin coaxing them through the complicated process of producing protective antibodies.
Vaccines are one of biomedicine’s most powerful and successful tools for protecting against infectious diseases. While we currently have safe and effective vaccines to prevent measles, mumps, and a great many other common childhood diseases, we still lack a vaccine to guard against respiratory syncytial virus (RSV)—a leading cause of pneumonia among infants and young children.
Each year, more than 2 million U.S. children under the age of 5 require medical care for pneumonia and other potentially life-threatening lower respiratory infections caused by RSV [1,2]. Worldwide, the situation is even worse, with more than 30 million infections estimated to occur annually, most among kids in developing countries, where as many as 200,000 deaths may result . So, I’m pleased to report some significant progress in biomedical research’s long battle against RSV: encouraging early results from a clinical trial of an experimental vaccine specifically designed to outwit the virus.