According to the Centers for Disease Control and Prevention (CDC), influenza is still widespread throughout the state of California and has resulted in a number of deaths, particularly among young children and seniors. Have you wondered why some have more susceptibility to these viruses? A new study by researchers affiliate with Carnegie Mellon University, Pittsburgh offers an explanation. It may be in your DNA. The researchers published their findings in the February 20 issue of JAMA.
The researchers focused on DNA sequences found on the end of chromosomes, known as telomeres. A telomere protects the end of the chromosome from deterioration or from fusion with neighboring chromosomes. Telomere regions deter the degradation of genes near the ends of chromosomes by allowing chromosome ends to shorten, which necessarily occurs during chromosome replication. Over time, due to each cell division, the telomere ends become shorter.
During cell division, enzymes that duplicate DNA cannot continue their duplication all the way to the end of chromosomes. If cells divided without telomeres, they would lose the ends of their chromosomes, and the necessary information they contain. The telomeres are disposable buffers blocking the ends of the chromosomes, are consumed during cell division, and are replenished by an enzyme, telomerase reverse transcriptase.
The researchers found that among healthy adults who were administered a cold virus, those with shorter telomere length in certain cells were more likely to develop experimentally-induced upper respiratory infection than participants with longer telomeres. Telomere shortening in leukocytes (white blood cells) has implications for immunocompetence and is associated with poorer antibody response to vaccines. The authors wrote: “Shorter leukocyte telomere length also is associated with aging-related illness and death from conditions with immune system involvement, including infectious diseases, cancer, and cardiovascular disease.” It is not known whether leukocyte telomere length is related to acute disease in younger, healthy populations.
Sheldon Cohen, PhD and his colleagues at Carnegie Mellon University conducted their study to determine whether shorter telomeres in leukocytes, especially CD8CD28- T cells, are associated with decreased resistance to upper respiratory infection and clinical illness in young to middle-aged adults. The study group comprised 152 healthy 18- to 55-year-old residents of Pittsburgh. Between 2008 and 2011, telomere length was assessed in peripheral blood mononuclear cells (PBMCs) and T-cell subsets (CD4, CD8CD28+, CD8CD28-). The participants were subsequently quarantined (single rooms), administered nasal drops containing a common cold virus (rhinovirus 39), and monitored for five days for development of infection and clinical illness.
The researcher found that 69% of participants (105) developed respiratory infections; 22% of the entire sample (33) developed a clinical illness (common cold).The researchers found that shorter telomere lengths in all four cell types were associated with increased odds of infection following exposure to RV39. However, CD8CD28- telomere length had the largest association with infection. The rate of infection in the CD8CD28- subset was 77% among participants in the group with the shortest telomeres and 50% for those in the group with the longest telomeres.
Analysis indicated that only telomere length in the CD8CD28- subset was associated with risk for clinical illness; shorter telomere length associated with increased risk. Among participants with the shortest telomeres, 26 percent became clinically ill. The rate for clinical illness was 13% for those in the group with the longest telomeres. Furthermore, the magnitude of the association between CD8CD28- telomere length and infection increased with increasing age.
The authors concluded, “In this study of healthy young and midlife adults, shorter CD8CD28- cell telomere length was associated with upper respiratory tract infection and clinical illness following experimental exposure to rhinovirus. Because these data are preliminary, their clinical implications are unknown.”