For nanomedicine, cell sex matters

New Emory/Georgia Tech BME faculty member Vahid Serpooshan's paper on the influences of cell sex on nanoparticle Read more

Toe in the water for Emory cryo-EM structures

Congratulations to Christine Dunham and colleagues in the Department of Biochemistry for their first cryo-electron microscopy paper, recently published in the journal Read more

Biomedical career fair April 13

We will provide more information when it is available. Friday, April 13. Emory Conference Center + Hotel, 1615 Read more


How Zika infects the placenta

Zika virus can infect and replicate in immune cells from the placenta, without killing them, scientists have discovered. The finding may explain how the virus can pass through the placenta of a pregnant woman, on its way to infect developing brain cells in her fetus.


Infected placental macrophages. Zika antigens visible in red. From Quicke et al (2016).

The results were published in Cell Host & Microbe.

“Our results substantiate the limited evidence from pathology case reports,” says senior author Mehul Suthar, PhD, assistant professor of pediatrics at Emory University School of Medicine. “It was known that the virus was getting into the placenta. But little was known about where the virus was replicating and in what cell type.”

Scientists led by Suthar and Emory pediatric infectious disease specialist Rana Chakraborty, MD, found that Zika virus could infect placental macrophages, called Hofbauer cells, in cell culture. The virus could also infect another type of placental cell, called cytotrophoblasts, but only after a couple days delay and not as readily. Other researchers recently reported that syncytiotrophoblasts, a more differentiated type of placental cell than cytotrophoblasts, are resistant to Zika infection.

The cells for the experiments were derived from full-term placentae, obtained from healthy volunteers who delivered by Cesarean section. The level of viral replication varied markedly from donor to donor, which hints that some women’s placentae may be more susceptible to viral infection than others. Read more

Posted on by Quinn Eastman in Immunology Leave a comment

Two angles on cell death

One can take two very different angles when approaching Bill Kaiser’s and Ed Mocarski’s work on RIP kinases and the mechanisms of cell death. These are: the evolutionary where-does-apoptosis-come-from angle, and the anti-inflammatory drug discovery angle.

A pair of papers published this week, one in PNAS and one in Journal of Immunology, cover both of these angles. (Also, back to back papers in Cell this week, originating from Australia and Tennessee, touch on the same topic.)

First, the evolutionary angle.

Cellular suicide can be a “scorched earth” defense mechanism against viruses. Kaiser and Mocarski have been amassing evidence that some forms of cellular suicide arose as a result of an arms race of competition with viruses. The PNAS paper is part of this line of evidence. It shows that the cell-death circuits controlled by three different genes (RIP1, RIP3 and caspase 8) apparently can be lifted cleanly out of an animal. Mice lacking all three genes not only can be born, but have well-functioning immune systems.

Apoptosis is thought to be a form of cellular suicide important for the development of all multicellular organisms. That’s why, to cell and developmental biologists, it seemed rather shocking that researchers can mutate a group of genes that drive apoptosis and other forms of cellular suicide and have adult animals emerge.

Next, the drug discovery angle.

The J. Immunol paper makes that angle clear enough. Most of the authors on this paper are from GlaxoSmithKline’s “Pattern Recognition Receptor Discovery Performance Unit, Immuno-Inflammation Therapeutic Area.” Here, they show that a mutation in RIP1 inactivating the kinase enzyme protects mice against severe skin and multiorgan inflammation. They conclude their abstract with: “Together, these data suggest that RIP1 kinase represents an attractive therapeutic target for TNF-driven inflammatory diseases.”

Note: TNF-driven inflammatory diseases include rheumatoid arthritis, inflammatory bowel diseases and psoriasis, representing a multibillion dollar market.


Posted on by Quinn Eastman in Immunology Leave a comment

Emory scientists co-signers of H5N1 flu letter

Emory influenza researchers Richard Compans, Anice Lowen and John Steel are co-signers of a statement announcing the end of a self-imposed moratorium on H5N1 avian flu research.

Last year, an international group of researchers called for the moratorium after public concern over studies of H5N1 transmissibility in ferrets, a model for spread of infection between humans. The group of researchers has now recommended ending the moratorium, citing safeguards and safety review procedures put in place by the National Institutes of Health and authorities in other countries. From the letter published today in Science and Nature:

In January 2012, influenza virus researchers from around the world announced a voluntary pause of 60 days on any research involving highly pathogenic avian influenza H5N1 viruses leading to the generation of viruses that are more transmissible in mammals. We declared a pause to this important research to provide time to explain the public-health benefits cheap oakley of this work, to describe the measures in place to minimize possible risks, and to enable organizations and governments around the world to review their policies (for example on biosafety, biosecurity, oversight, and communication) regarding these experiments.

…Thus, acknowledging that the aims of the voluntary moratorium have been met in some countries and are close to being met in others, we declare an end to the voluntary moratorium on avian flu transmission studies.

Dan Vergano has a more extensive story in USA Today.

Compans is professor of microbiology and immunology at Emory University School of Medicine and scientific director of Emory’s Influenza Pathogenesis and Immunology Research Center. Lowen and Steel are assistant professors of microbiology and immunology at Emory and IPIRC investigators.

Posted on by Quinn Eastman in Immunology Leave a comment

A family of troublemakers known as XMRV

A long-delayed paper on the connection between chronic fatigue syndrome and XMRV (xenotropic murine leukemia virus-related virus) finally surfaced last week in PNAS. Astute readers may recall that XMRV has also been linked to prostate cancer.

Detecting XMRV in prostate tissue. A variety of assays (neutralizing antibodies, polymerase chain reaction or fluorescence in situ hybridization) may be used to look for XMRV

The twist from last week’s paper is that the NIH/FDA team, led by Harvey Alter, didn’t find viruses all with the same sequence in chronic fatigue patients. Instead, they found a cluster of closely related, but different, viruses. While confusing, these results may explain why tests for the presence of the virus that are based on viral DNA sequences may have generated varying (and conflicting) results. An alternative assay based on antibodies, such as the one urologist John Petros and colleagues at Emory developed, may be useful because it casts a wider net.

Pathologist Hinh Ly has been diving into the XMRV field, with a recent paper in Journal of Virology describing what “gateway” (receptor) molecule the virus uses to sneak into cells and what kinds of cells in the prostate it can infect.

In a collaboration with Ila Singh at the University of Utah, antiviral drug expert Raymond Schinazi has found that a number of drugs active against HIV also stop XMRV. This offers some hope that if doctors can detect members of the XMRV family, and figure out what they’re up to, they might be able to combat the troublemakers as well.

Posted on by Quinn Eastman in Uncategorized Leave a comment