Cold sores may be tied to memory loss, study suggests

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Cold sores may be tied to memory loss, study suggests

By Steve James, NBC News contributor

Researchers have found that the virus that causes cold sores, along with other viral or bacterial infections, might be associated with memory loss, and if further studies establish such a link, it could eventually prove helpful in preventing strokes or Alzheimer’s disease.

A long-term study of a group of people in one neighborhood of New York City found that those with higher levels of infection in their blood -- meaning they had been exposed to various pathogens such as the herpes simplex type 1 virus that causes cold sores -- were more likely to have cognitive problems than people with lower levels of infection in the blood. The results, released Monday, are published in the March 26 issue of Neurology, the medical journal of the American Academy of Neurology....

The study, performed in collaboration with the Miller School of Medicine at the University of Miami, tested thinking and memory in 1,625 people from northern Manhattan who had an average age of 69. Participants gave blood samples that were tested for five common low grade infections: three viruses (herpes simplex type 1, which is oral; herpes simplex type 2, which is genital; and cytomegalovirus), chlamydia pneumoniae (a common respiratory infection) and Helicobacter pylori (a bacteria found in the stomach).

This is the study:
Infectious burden and cognitive function

The Northern Manhattan Study

1. Mira Katan, MD,
2. Yeseon Park Moon, MS,
3. Myunghee Cho Paik, PhD,
4. Ralph L. Sacco, MD, MS,
5. Clinton B. Wright, MD and
6. Mitchell S.V. Elkind, MD, MS

1. Correspondence to Dr. Katan: mk3270@columbia.edu

1. doi: 10.1212/WNL.0b013e3182896e79 Neurology March 26, 2013 vol. 80 no. 13 1209-1215

Objective: We hypothesized that infectious burden (IB), a composite serologic measure of exposure to common pathogens (i.e., Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpes simplex virus 1 and 2) associated with vascular risk in the prospective Northern Manhattan Study (NOMAS), would also be associated with cognition.

Methods: Cognition was assessed using the Mini-Mental State Examination (MMSE) at enrollment and the modified Telephone Interview for Cognitive Status (TICS-m) at annual follow-up visits. Adjusted linear and logistic regressions were used to measure the association between IB index and MMSE. Generalized estimating equation models were used to evaluate associations with TICS-m and its change over time.

Results: Serologies and cognitive assessments were available in 1,625 participants of the NOMAS cohort. In unadjusted analyses, higher IB index was associated with worse cognition (change per standard deviation [SD] of IB for MMSE was −0.77, p < 0.0001, and for first measurements of TICS-m was −1.89, p < 0.0001). These effects were attenuated after adjusting for risk factors (for MMSE adjusted change per SD of IB = −0.17, p = 0.06, for TICS-m adjusted change per SD IB = −0.68, p < 0.0001). IB was associated with MMSE ≤24 (compared to MMSE >24, adjusted odds ratio 1.26 per SD of IB, 95% confidence interval 1.06–1.51). IB was not associated with cognitive decline over time. The results were similar when IB was limited to viral serologies only.

Conclusion: A measure of IB associated with stroke risk and atherosclerosis was independently associated with cognitive performance in this multiethnic cohort. Past infections may contribute to cognitive impairment.

Note: An earlier viral study with results on other health issues as most ME/CFS patients have high titers of EBV, HHV6, CMV, Parvovirus B19, etc.


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For the more scientific types who want to dig into this of long term infections impairing the immune response read below or the PDF. For the non scientific types the answer is a strong correlation.

Cytomegalovirus Infection Impairs Immune Responses and Accentuates T-cell Pool Changes Observed in Mice with Aging

Author Summary

The cytomegalovirus (CMV) is a widespread virus of the herpesvirus family, which latently infects the majority of the adult human population worldwide. While CMV causes severe disease in AIDS patients, in recipients of organ transplants, or when infection occurs during pregnancy, this virus is considered apathogenic for the general population. Several reports indicated that CMV infection may be associated with poor immune function, and even survival, in older adults, yet it remained unclear whether CMV infection may have the potential to impair the immune function. Here we test this possibility in a mouse model of CMV (MCMV) infection.

We found that mice carrying latent MCMV exhibit significant changes in CD8+ lymphocytes, which are crucial in the recognition of, and protection against viruses. These changes were similar to changes observed in aging and resulted in poor cytotoxic T-lymphocyte response to infection with unrelated viruses, such as the West Nile virus or the influenza virus. Our study provides the first experimental demonstration that latent CMV infection may impair the immune defense of the host.

Also​

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Lifelong persistent viral infection alters the naive T cell pool, impairing CD8 T cell immunity in late life.​

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Smithey MJ, Li G, Venturi V, Davenport MP, Nikolich-Žugich J.
Source

Department of Immunobiology, University of Arizona College of Medicine, Tucson, AZ 85724, USA.
Abstract

Persistent CMV infection has been associated with immune senescence. To address the causal impact of lifelong persistent viral infection on immune homeostasis and defense, we infected young mice systemically with HSV-1, murine CMV, or both viruses and studied their T cell homeostasis and function. Herpesvirus(+) mice exhibited increased all-cause mortality compared with controls. Upon Listeria-OVA infection, 23-mo-old animals that had experienced lifelong herpesvirus infections showed impaired bacterial control and CD8 T cell function, along with distinct alterations in the T cell repertoire both before and after Listeria challenge, compared with age-matched, herpesvirus-free controls.

Herpesvirus infection was associated with reduced naive CD8 T cell precursors above the loss attributable to aging. Moreover, the OVA-specific CD8 T cell repertoire recruited after Listeria challenge was entirely nonoverlapping between control and herpesvirus(+) mice. To our knowledge, this study for the first time causally links lifelong herpesvirus infection to all-cause mortality in mice and to disturbances in the T cell repertoire, which themselves correspond to impaired immunity to a new infection in aging.

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