title: Interaction between infectious diseases and personality traits: ACP1*C as a potential mediator.
abstract: In geographical regions characterized by high pathogen prevalence, it has been shown that human populations tend to be characterized by lower levels of extraversion (E) and openness to experience (OtE). According to the "behavioral immune system" hypothesis, the reduction of extraversion and openness levels represents a behavioral defense against infections. Like the 'classical' immune system, the "behavioral immune system" could also be shaped by its underlying genetic background. Previous studies have shown that the *C allele of the ACP1 gene confers increased susceptibility to infectious/parasitic diseases. We hypothesized that carriers of the ACP1*C allele should likewise be associated with reduced E and OtE. We tested this hypothesis using two samples comprised of 153 students from Southern California (Group 1), and 162 female subjects recruited from an executive health program (Group 2), genotyped for ACP1 polymorphism and evaluated by the NEO Five-Factor Inventory (NEO-FFI). ACP1 was significantly associated with E: we found that carriers of ACP1*C showed reduced scores for E (Group 1: β=-4.263, P=0.027; Group 2: β=-8.315, P=0.003; Group 1+Group 2: β=-5.366, P=0.001). Across groups, ACP1 was only marginally associated with OtE. In conclusion, the present study found that the ACP1*C allele, previously associated with an increased vulnerability to infectious/parasitic diseases may also be able to shape behavioral immune defenses by interaction with the level of E.
authors.affiliation: Innovation Pole for Genomics, Genetics and Biology, Perugia, Italy. Electronic address: napvale@gmail.com.
authors.forename: Valerio
authors.initials: V
authors.lastname: Napolioni
authors.affiliation: Department of Psychology, University of California, Los Angeles, CA, USA.
authors.forename: Damian R
authors.initials: DR
authors.lastname: Murray
authors.affiliation: City of Hope National Medical Center, Duarte, CA, USA.
authors.forename: David E
authors.initials: DE
authors.lastname: Comings
authors.affiliation: Center for Health Promotion, Loma Linda University School of Medicine, Loma Linda, CA, USA.
authors.forename: Warren R
authors.initials: WR
authors.lastname: Peters
authors.affiliation: Genetic Research Institute of the Desert, Rancho Mirage, CA, USA.
authors.forename: Radhika
authors.initials: R
authors.lastname: Gade-Andavolu
authors.affiliation: Carlsbad Science Foundation, Monrovia, CA, USA.
authors.forename: James
authors.initials: J
authors.lastname: MacMurray
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D003141:Communicable Diseases / Q000453:epidemiology / Q000209:etiology*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D010551:Personality; D020641:Polymorphism, Single Nucleotide; D017027:Protein Tyrosine Phosphatases / Q000235:genetics; D011518:Proto-Oncogene Proteins / Q000235:genetics; D019655:Quantitative Trait, Heritable; D055815:Young Adult
chemical_list: D011518:Proto-Oncogene Proteins; C490429:ACP1 protein, human; D017027:Protein Tyrosine Phosphatases
keywords: ACP1; Behavior; Genetics; Infectious disease; Personality trait; Polymorphism