Scientists discover why newborns get sick so often

October 31, 2013

If you think cold and flu season is tough, trying being an infant. A new research finding published in the November 2013 issue of the Journal of Leukocyte Biology sheds new light on why newborns appear to be so prone to getting sick with viruses—they are born without one of the key proteins needed to protect them. This protein, called "toll-like receptor 3" or "TLR3," is involved in the recognition of different viruses and mediates the immune response to them. Without this protein, newborn immune cells are not equipped to recognize and react appropriately to certain viruses, in particular, the herpes simplex virus known as HSV.

"This study helps to understand the molecular basis for the immaturity of the immune system of newborns, which we believe will contribute to development of therapeutic interventions to protect this vulnerable population group," said Lucija Slavica, a researcher involved in the work from the Department of Rheumatology and Inflammation Research at the University of Gothenburg in Gothenburg, Sweden.

To make this discovery, scientists compared from the cord blood of newborns with the same type of from adults. The cells from newborns did not contain the protein TLR3, which was present in adult cells. These cells rid the body of viral-infected cells, ultimately eliminating viral infections. When researchers treated both cell groups with a synthetic component mimicking a viral presence, the adult reacted by secreting substances involved in immune reaction against viruses (interferon-gamma) and killed cells infected with virus, while cells from could not do this or were impaired in performing this function.

"This study adds to the growing body of research stemming from the Nobel-winning discovery in 2011 on how the immune system recognizes microbes by shedding light on how these pathways develop over time after birth," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "This report is particularly important - as any new parent can attest, infants are particularly susceptible to infections and understanding which pathways are not yet functional could lead to novel therapies."

Explore further: Study provides new knowledge about the body's fight against HIV

More information: Lucija Slavica, Inger Nordström, Merja Nurkkala Karlsson, Hadi Valadi, Marian Kacerovsky, Bo Jacobsson, and Kristina Eriksson.
TLR3 impairment in human newborns. J Leukoc Biol. November 2013 94:1003-1011; DOI: 10.1189/jlb.1212617

Related Stories

Study provides new knowledge about the body's fight against HIV

October 31, 2013
A study of the body's reactions to the HIV virus by Danish researchers has led to new understanding of the immune system's fight against HIV. The discovery is an important step on the road towards the future development of ...

Pregnant women with hepatitis C may pass heartier viral strain to newborns, study suggests

October 28, 2013
Infants who get hepatitis C from their mothers during childbirth may inherit a viral strain that replicates more quickly than strains found in non-pregnant hosts, according to a new study published Oct. 27 in Nature Medicine. ...

How and why herpes viruses reactivate to cause disease

October 31, 2012
The mere mention of the word "herpes" usually conjures negative images and stereotypes, but most people have been infected with some form of the virus. For most, a sore appears, heals and is forgotten, although the virus ...

Immune system discovery could lead to EBV vaccine to prevent mono, some cancers

October 11, 2013
Development of a vaccine against Epstein-Barr virus (EBV) has taken a step forward with the Canadian discovery of how EBV infection evades detection by the immune system.

New target to fight HIV infection identified

October 1, 2013
A mutant of an immune cell protein called ADAP (adhesion and degranulation-promoting adaptor protein) is able to block infection by HIV-1 (human immunodeficiency virus 1), new University of Cambridge research reveals. The ...

Researchers identify vulnerabilities of the deadly Ebola virus

July 23, 2013
Disabling a protein in Ebola virus cells can stop the virus from replicating and infecting the host, according to researchers from the Icahn School of Medicine at Mount Sinai. The data are published in July in the journal ...

Recommended for you

Molecular hitchhiker on human protein signals tumors to self-destruct

July 24, 2017
Powerful molecules can hitch rides on a plentiful human protein and signal tumors to self-destruct, a team of Vanderbilt University engineers found.

New vaccine production could improve flu shot accuracy

July 24, 2017
A new way of producing the seasonal flu vaccine could speed up the process and provide better protection against infection.

Researchers develop new method to generate human antibodies

July 24, 2017
An international team of scientists has developed a method to rapidly produce specific human antibodies in the laboratory. The technique, which will be described in a paper to be published July 24 in The Journal of Experimental ...

A sodium surprise: Engineers find unexpected result during cardiac research

July 20, 2017
Irregular heartbeat—or arrhythmia—can have sudden and often fatal consequences. A biomedical engineering team at Washington University in St. Louis examining molecular behavior in cardiac tissue recently made a surprising ...

Want to win at sports? Take a cue from these mighty mice

July 20, 2017
As student athletes hit training fields this summer to gain the competitive edge, a new study shows how the experiences of a tiny mouse can put them on the path to winning.

'Smart' robot technology could give stroke rehab a boost

July 19, 2017
Scientists say they have developed a "smart" robotic harness that might make it easier for people to learn to walk again after a stroke or spinal cord injury.

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.