Interview with Dr. Anthony Fauci on “Mississippi Baby



In an important announcement, Thursday, July 10, the National Institutes of Health (NIH) reported that the child known as the “Mississippi Baby”—an infant seemingly cured of HIV after treatment had been initiated within hours of birth—now has detectable levels of HIV after more than two years of not taking antiretroviral therapy without evidence of the virus.

To learn more, sat down with Dr. Anthony Fauci, Director of the National Institutes of Allergy and Infectious Diseases (NIAID), and asked him to share with us what this development means for our understanding of the intricacies of HIV infection and how it may affect HIV research efforts moving forward. NIAID and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), both part of NIH, provided funding to the researchers involved in the analysis of the case.

Click here to watch the interview.

We are very thankful that the more we learn, the more we can move forward. We are also thankful that all reports indicate that the child is well under the ongoing care of an excellent team of pediatric HIV specialists. We remain optimistic for the future as we continue to pursue the goals of the National HIV/AIDS Strategy and to support groundbreaking research that is giving us the tools to move towards an AIDS-free generation.

By Ronald Valdiserri, M.D., M.P.H., Deputy Assistant Secretary for Health, Infectious Diseases, and Director, Office of HIV/AIDS and Infectious Disease Policy, U.S. Department of Health and Human Services


HIV study leads to insights into deadly infection

Research led by the University of Adelaide has provided new insights into how the HIV virus greatly boosts its chances of spreading infection, and why HIV is so hard to combat.

HIV infects human immune cells by turning the infection-fighting proteins of these cells into a “backdoor key” that lets the virus in. Recent research has found that another protein is involved as well. A peptide in semen that sticks together and forms structures known as “amyloid fibrils” enhances the virus’s infection rate by up to an astonishing 10,000 times.

How and why these fibrils enhance infection and cause toxicity in the body’s cells remains unknown.

The HIV fibrils — known as “semen-derived enhancers of viral infection” (SEVI) — have been studied by chemistry and pharmacology researchers at the University of Adelaide. The results of this work have now been published online in the journal Biochimica et Biophysica Acta.

“Amyloid fibrils play an important role in a number of prominent diseases, such as Parkinson’s, Alzheimer’s and others, and it’s absolutely essential that we understand how they work if we have any hope of developing new drugs to stop them,” says lead author Dr Ian Musgrave, from the University’s School of Medical Sciences.

In laboratory studies, the team found that the HIV fibrils are toxic towards cells from the nervous system. They also found that even when the fibril is broken apart, its constituent elements continue to be toxic.

“This suggests that you can’t just prevent one part of SEVI from aggregating and being toxic to cells. You need to shut the whole thing down or stop it from forming in the first place,” Dr Musgrave says.

Researchers also tested the fibrils against another major type of body tissue, epithelial cells, and found they were not toxic to these cells.

“Epithelial cells are a major barrier to HIV entry. There have been theories that the fibrils can damage the epithelial layer, making it much easier for the virus to enter the body and infect the immune cells, but our findings show that healthy epithelial cells are resistant,” Dr Musgrave says.

“This is an important finding because it could mean that the toxicity from the fibrils is dependent on the type of tissue they come in contact with,” Dr Musgrave says.

“We now have a better understanding of the role of these protein enhancers in HIV infection. However, it’s clear that much more research is needed in this area,” he says.

Story Source:

The above story is based on materials provided by University of Adelaide. Note: Materials may be edited for content and length.

Journal Reference:

  1. Abigail K. Elias, Denis Scanlon, Ian F. Musgrave, John A. Carver. SEVI, the semen enhancer of HIV infection along with fragments from its central region, form amyloid fibrils that are toxic to neuronal cells. Biochimica et Biophysica Acta (BBA) – Proteins and Proteomics, 2014; 1844 (9): 1591 DOI: 10.1016/j.bbapap.2014.06.006

PMBSGN & Healthy HIV & Pozitively Healthy Coalition (NSC), Mourning the crash of Malaysia Airline flight MH17

(Clockwise from top left: Flowers left at AIDS 2014 Welcome Sign; Dr. Joep Lange; Jacqueline van Tageren; Lucie van Mens; Martine de Schutter; Pim de Kuijer; and Glenn Raymond Thomas)Memory of Our Colleagues:

HealthHIV and the Pozitively Healthy Coalition join the world in mourning the crash of Malaysia Airline flight MH17 which tragically claimed the lives of many members of the global AIDS community.

HealthHIV had the honor of working with Dr. Joep Lange, former president of the International AIDS Society, who died with his partner, Jacqueline van Tongeren, a board member of ArtAids. Other members of the AIDS community lost include Glenn Raymond Thomas, a World Health Organization spokesperson and former BBC journalist; Pim de Kuijer, an activist with Stop AIDS Now and AIDS Fund Netherlands; Martine de Schutter, a program manager at Bridging the Gaps; and Lucie van Mens, director of program development and support with the Female Health Company.  

We will endeavor to honor their innovation and advocacy to improve the health and well-being of those living with and impacted by HIV around the world. Our thoughts and prayers are with their families, friends, and colleagues.