The main question of this article is: “Despite its negative consequences, why does depression persist in the population?” The article introduces the “infection-defense hypothesis” of depression, which proposes that moods—with their ability to orchestrate a wide array of physical and behavioral responses—have played an adaptive role throughout human history by helping individuals fight existing infections, as well as helping both individuals and their kin avoid new ones. In contrast to many previous evolutionary theories of depression, the infection-defense hypothesis takes into account and helps to integrate a large and growing body of evidence linking depression to inflammation and immune function, and helps to explain depression’s association with a vast array of conditions and illnesses such as nutritional deficiencies, seasonal changes, hormonal fluctuations, and chronic diseases. The article also notes several predictions for the infection-defense hypothesis. Predictions include: (1) most signs and symptoms of depression will aid the immune system’s ability to fight infections, by performing one or more of the following functions, (2) many types of infectious diseases will be associated with depressive symptoms, (3) depressed individuals will tend to have elevated rates of infection and/or immune alteration, (4) medical, environmental, and physiological conditions that increase immune vulnerability, or that increase exposure to infection, will also be associated with increased rates of depression, (5) there are bidirectional processes that communicate between the nervous and immune systems and provide mechanisms for infections, immune processes, and mood to influence one another, and (6) moods provide an implicit mechanism for cost-benefit analysis of an individual’s optimal responses to environmental challenges and the organisms’ immune status, helping to regulate the timing and intensity of infection-defense responses. Considerable evidence exists to support each of these predictions. The infection-defense hypothesis and in particular, the notion that moods may serve as a behavioral defense against infection, can possibly play a role in understanding the causes, treatment, and prevention of depression.

Link: http://web.a.ebscohost.com.proxy.library.emory.edu/ehost/detail?sid=ca4e29eb-500c-4354-94de-cc3144e48bd3%40sessionmgr4005&vid=7&hid=4204

The article’s main question is: “what is the influence of major histocompatibility complex (MHC) on patterns of reproduction in the mandrill? The study also looked into the possibility of whether or not the males had a reproductive advantage via either superior competitive ability or via female choice within-male MHC diversity. This study is innovative because this particular study contained a large dataset, involving reproduction over multiple years for a long-lived species. This study was also the first to demonstrate a reproductive advantage associated with MHC dissimilarity in a polygynous species with high levels of male-male competition. This study supported previous studies showing significantly higher rate of nonsynonymous than synonymous substitutions within the mandrill DRB.

This study was done on a large, semi-free-ranging population of mandrills, at the Centre International de Recherches Médicales, Franceville. Observations of the female reproductive status, births, injuries, and disappearance were made daily. DNA was extracted from blood samples obtained during annual captures of the colony for genetic analysis. MHC-DRB genotyping was also conducted for 155 of the population. The overall genetic similarity between genotypes of two individuals was estimated in order to determine whether reproduction was biased towards unrelated partners. Measures of MHC dissimilarity were also calculated for each potentially reproductive dyad in order to determine whether reproduction was biased towards partners with dissimilar MHC genotypes. Various statistical analyses were done in order to answer questions such as, “does overall genetic dissimilarity influence reproduction?” or “does male genotype influence reproduction?”

After genetic analysis, the results suggest that the MHC sequences are capable of providing resistance to pathogens, and thus might be the foundation of MHC- associated mate choice. The results showed that that pedigree relatedness, overall genetic dissimilarity, MHC dissimilarity and male genotype all influenced reproduction in this mandrill colony. Results also showed that male rank was by far the strongest influence on reproduction in males, with alpha males being 18 times more likely to sire a given offspring than nonalpha males.

The findings show that MHC-associated mate choice may be more widespread than previously thought. The findings also suggest that individual genetic characteristics in mandrills may be linked to male vigour and further studies can be taken on to investigate whether microsatellite heterozygosity or MHC diversity are linked to better condition or reduced susceptibility to disease.

The main question of this article is: “What are the evolutionary features of human neurodegenerative disease genes with respect to non-disease genes?” Through analysis of gene expression level, number of regulatory miRNAs, protein connectivity, intrinsic disorder content, and relative aggregation propensity, Panda et al. observed that human neurodegenerative disease genes are evolutionary conserved relative to non-disease genes. Statistical analyses were performed using SPSS v.13. Mann-Whitney U test was used to compare the average values of different variables between two classes of genes. For correlation analysis, the Spearman’s Rank correlation co- efficient was performed. They also observed that human neurodegenerative disease genes have higher number of different regulatory miRNAs target sites and also have higher interaction partners than the non-disease genes. Overall, results showing higher gene expression level, higher protein connectivity along with greater miRNA regulation of neurodegenerative disease genes compared to non-disease genes support the conserved nature of neurodegenerative disease genes. In particular, highest (P=0.0001) expression of neurodegenerative disease genes were found near nervous system related tissues. In addition, it was found that non-disease genes on average show uniform gene expression level within the range of 25–60 whereas, for neurodegenerative disease genes the inhomogeneous expression level often fluctuates within the range of 25–150. Not only have the evolutionary features of human neurological disorders have been identified, but the complicated relationships between protein disorder content and RAP have been clarified. An implication of this study is that these results can be used in order to diagnose, prevent, and treat neurological disorders.

Link to article: http://web.a.ebscohost.com.proxy.library.emory.edu/ehost/pdfviewer/pdfviewer?vid=7&sid=ca4e29eb-500c-4354-94de-cc3144e48bd3%40sessionmgr4005&hid=4204

Many found it interesting that the prevalence of H. pylori infections did not correlate with cancer incidence. In a study of two Colombian populations, a coastal population of African ancestry had a low incidence of gastric cancer compared to a population of largely Amerindian descent in the Andes Mountains. By studying the tissue samples of patients from these populations, molecular biologists and researchers found out that the H. pylori strain affecting those in the coastal region were of African descent, while the H. pylori strain affecting the Amerindian human population were of south European descent. The results demonstrated that a “shared evolutionary history of humans and bacteria resulted in a less virulent host-pathogen relationship.”

“[It’s] fascinating,” said El-Omar. “If you have African strains affecting African-ancestry hosts, it doesn’t cause too much damage, whereas if you’ve got African-origins strains infecting Amerindians up in the mountains, that’s when you get most precancerous changes. So it looks like if you’ve coevolved with your strains, you get less and less virulence.”

This article didn’t go into too much detail about the evolutionary mechanisms so I did some more research on this host-pathogen coevolution. I found out that one explanation for why one population is more affected by diseases is tolerance evolution. The evolution of tolerance results in a changed selection on parasite populations, which can lead to parasite evolution despite the fact that tolerance is not directly antagonistic to parasite fitness. The evolution of tolerance is like our attempts of vaccination in order to decrease the prevalence of disease, without reducing parasite densities or eradicating the infection. These vaccinations can select for more pathogenic viruses, creating a greater risk for those unvaccinated who come into contact with these pathogens. Tolerant individuals also select for parasites with greater virulence, causing a more devastating effect on those intolerant who become exposed to the disease.

Link to article: http://www.the-scientist.com/?articles.view/articleNo/38845/title/Human-Pathogen-Coevolution/