The evolution of early hominin food production and sharing.

How did humans evolve from individualistic to collective foraging with sex differences in production and widespread sharing of plant and animal foods? While current evolutionary scenarios focus on meat, cooking, or grandparental subsidies, considerations of the economics of foraging for extracted plant foods (e.g., roots, tubers), inferred to be important for early hominins (∼6 to 2.5 mya), suggest that early hominins shared such foods with offspring and others. Here, we present a conceptual and mathematical model of early hominin food production and sharing, prior to the emergence of frequent hunting, cooking, and increased lifespan. We hypothesize that extracted plant foods were vulnerable to theft, and that male mate guarding protected females from food theft. We identify conditions favoring extractive foraging and food sharing across mating systems (i.e., monogamy, polygyny, promiscuity), and we assess which system maximizes female fitness with changes in the profitability of extractive foraging. Females extract foods and share them with males only when: i) extracting rather than collecting plant foods pays off energetically; and ii) males guard females. Males extract foods when they are sufficiently high in value, but share with females only under promiscuous mating and/or no mate guarding. These results suggest that if early hominins had mating systems with pair-bonds (monogamous or polygynous), then food sharing by adult females with unrelated adult males occurred before hunting, cooking, and extensive grandparenting. Such cooperation may have enabled early hominins to expand into more open, seasonal habitats, and provided a foundation for the subsequent evolution of human life histories.

A Mutation in the UL24 Gene Abolishes Expression of the Newly Identified UL24.5 Protein of Herpes Simplex Virus 1 and Leads to an Increase in Pathogenicity in Mice.

Herpes simplex virus 1 (HSV-1) infects the host via epithelia and establishes latency in sensory neurons. The UL24 gene is conserved throughout the Herpesviridae family, and the UL24 protein is important for efficient viral replication and pathogenesis. Multiple transcripts are expressed from the UL24 gene. The presence of a transcription initiation site inside the open reading frame of UL24 and an ATG start codon in the same open reading frame led us to suspect that another protein was expressed from the UL24 locus. To test our hypothesis, we constructed a recombinant virus that expresses a hemagglutinin tag at the C terminus of UL24. Western blot analysis revealed the expression of an 18-kDa protein that is not a degradation product of the full-length UL24, which we refer to as UL24.5. Ectopically expressed UL24.5 did not induce the dispersal of nucleolar proteins, as seen for UL24. In order to characterize the role of UL24.5, we constructed a mutant virus encoding a substitution of the predicted initiation methionine to a valine. This substitution eliminated the expression of the 18-kDa polypeptide. Unlike the UL24-null mutant (UL24X), which exhibits reduced viral yields, the UL24.5-null mutant exhibited the same replication phenotype in cell culture as the parental strain. However, in a murine ocular infection model, we observed an increase in the incidence of neurological disorders with the UL24.5 mutant. Alignment of amino acid sequences for various herpesviruses revealed that the initiation site of UL24.5 is conserved among HSV-1 strains and is present in many herpesviruses.IMPORTANCE We discovered a new HSV-1 protein, UL24.5, which corresponds to the C-terminal portion of UL24. In contrast to the replication defects observed with HSV-1 strains that do not express full-length UL24, the absence of UL24.5 did not affect viral replication in cell culture. Moreover, in mice, the absence of UL24.5 did not affect viral titers in epithelia or trigeminal ganglia during acute infection; however, it was associated with a prolonged persistence of signs of inflammation. Strikingly, the absence of UL24.5 also led to an increase in the incidence of severe neurological impairment compared to results for wild-type control viruses. This increase in pathogenicity is in stark contrast to the reduction in clinical signs associated with the absence of full-length UL24. Bioinformatic analyses suggest that UL24.5 is conserved among all human alphaherpesviruses and in some nonhuman alphaherpesviruses. Thus, we have identified UL24.5 as a new HSV-1 determinant of pathogenesis.

Learning to Cooperate: The Evolution of Social Rewards in Repeated Interactions.

Understanding the behavioral and psychological mechanisms underlying social behaviors is one of the major goals of social evolutionary theory. In particular, a persistent question about animal cooperation is to what extent it is supported by other-regarding preferences-the motivation to increase the welfare of others. In many situations, animals adjust their behaviors through learning by responding to the rewards they experience as a consequence of their actions. Therefore, we may ask whether learning in social situations can be driven by evolved other-regarding rewards. Here we develop a mathematical model in order to ask whether the mere act of cooperating with a social partner will evolve to be inherently rewarding. Individuals interact repeatedly in pairs and adjust their behaviors through reinforcement learning. We assume that individuals associate with each game outcome an internal reward value. These perceived rewards are genetically evolving traits. We find that conditionally cooperative rewards that value mutual cooperation positively but the sucker's outcome negatively tend to be evolutionarily stable. Purely other-regarding rewards can evolve only under special parameter combinations. On the other hand, selfish rewards that always lead to pure defection are also evolutionarily successful. These findings are consistent with empirical observations showing that humans tend to display conditionally cooperative behavior and also exhibit a diversity of preferences. Our model also demonstrates the need to further integrate multiple levels of biological causation of behavior.

Dok-1 and Dok-2 Are Required To Maintain Herpes Simplex Virus 1-Specific CD8+ T Cells in a Murine Model of Ocular Infection.

Dok-1 and Dok-2 negatively regulate responses downstream of several immune receptors in lymphoid and myeloid cells. Recent evidence showed that Dok proteins are essential in the formation of memory CD8+ T cells to an exogenous epitope expressed by vaccinia virus; however, the importance of Dok-1 and Dok-2 in the control of viral infection is unknown. Here, we investigated the role of Dok proteins in modulating the immune response against herpes simplex virus 1 (HSV-1) in a mouse model of ocular infection. During acute infection, viral titers in the eye were similar in wild-type (WT) and Dok-1 and Dok-2 double-knockout (DKO) mice, and the percentages of infiltrating leukocytes were similar in DKO and WT corneas and trigeminal ganglia (TG). DKO mice exhibited a diminished CD8+ T cell response to the immunodominant HSV-1 glycoprotein B (gB) epitope in the spleen and draining lymph nodes compared to WT mice during acute infection. Remarkably, gB-specific CD8+ T cells almost completely disappeared in the spleens of DKO mice during latency, and the reduction of CD8+ effector memory T (Tem) cells was more severe than that of CD8+ central memory T (Tcm) cells. The percentage of gB-specific CD8+ T cells in TG during latency was also dramatically reduced in DKO mice; however, they were phenotypically similar to those from WT mice. In ex vivo assays, reactivation was detected earlier in TG cultures from infected DKO versus WT mice. Thus, Dok-1 and Dok-2 promote survival of gB-specific CD8+ T cells in TG latently infected with HSV-1.IMPORTANCE HSV-1 establishes lifelong latency in sensory neurons of trigeminal ganglia (TG). In humans, HSV-1 is able to sporadically reactivate from latently infected neurons and establish a lytic infection at a site to which the neurons project. Most herpetic disease in humans is due to reactivation of HSV-1 from latency rather than to primary acute infection. CD8+ T cells are thought to play an important role in controlling recurrent infections. In this study, we examined the involvement of Dok-1 and Dok-2 signaling proteins in the control of HSV-1 infection. We provide evidence that Dok proteins are required to maintain a CD8+ T cell response against HSV-1 during latency-especially CD8+ Tem cells-and that they negatively affect HSV-1 reactivation from latency. Elucidating Dok-mediated mechanisms involved in the control of HSV-1 reactivation from latency might contribute to the development of therapeutic strategies to prevent recurrent HSV-1-induced pathology.

On learning dynamics underlying the evolution of learning rules.

In order to understand the development of non-genetically encoded actions during an animal's lifespan, it is necessary to analyze the dynamics and evolution of learning rules producing behavior. Owing to the intrinsic stochastic and frequency-dependent nature of learning dynamics, these rules are often studied in evolutionary biology via agent-based computer simulations. In this paper, we show that stochastic approximation theory can help to qualitatively understand learning dynamics and formulate analytical models for the evolution of learning rules. We consider a population of individuals repeatedly interacting during their lifespan, and where the stage game faced by the individuals fluctuates according to an environmental stochastic process. Individuals adjust their behavioral actions according to learning rules belonging to the class of experience-weighted attraction learning mechanisms, which includes standard reinforcement and Bayesian learning as special cases. We use stochastic approximation theory in order to derive differential equations governing action play probabilities, which turn out to have qualitative features of mutator-selection equations. We then perform agent-based simulations to find the conditions where the deterministic approximation is closest to the original stochastic learning process for standard 2-action 2-player fluctuating games, where interaction between learning rules and preference reversal may occur. Finally, we analyze a simplified model for the evolution of learning in a producer-scrounger game, which shows that the exploration rate can interact in a non-intuitive way with other features of co-evolving learning rules. Overall, our analyses illustrate the usefulness of applying stochastic approximation theory in the study of animal learning.

Human ability to detect kinship in strangers' faces: effects of the degree of relatedness.

The resemblance between human faces has been shown to be a possible cue in recognizing the relatedness between parents and children, and more recently, between siblings. However, the general inclusive fitness theory proposes that kin-selective behaviours are also relevant to more distant relatives, which requires the detection of larger kinship bonds. We conducted an experiment to explore the use of facial clues by 'strangers', i.e. evaluators from a different family, to associate humans of varying degrees of relatedness. We hypothesized that the visual capacity to detect relatedness should be weaker with lower degrees of relatedness. We showed that human adults are capable of (although not very efficient at) assessing the relatedness of unrelated individuals from photographs and that visible facial cues vary according to the degree of relatedness. This sensitivity exists even for kin pair members that are more than a generation apart and have never lived together. Collectively, our findings are in agreement with emerging knowledge on the role played by facial resemblance as a kinship cue. But we have progressed further to show how the capacity to distinguish between related and non-related pairs applies to situations relevant to indirect fitness.

Regulation of viral gene expression by the herpes simplex virus 1UL24 protein (HSV-1UL24 inhibits accumulation of viral transcripts).

UL24 is conserved among all Herpesviridae. In herpes simplex virus 1 (HSV-1), UL24 mutations lead to reduced viral titers both in cell culture and in vivo, and reduced pathogenicity. The human cytomegalovirus ortholog of UL24 has a gene regulatory function; however, it is not known whether other UL24 orthologs also affect gene expression. We discovered that in co-transfection experiments, expression of UL24 correlated with a reduction in the expression of several viral proteins and transcripts. Substitution mutations targeting conserved residues in UL24 impaired this function. Reduced transcript levels did not appear attributable to changes in mRNA stability. The UL24 ortholog of Herpes B virus exhibited a similar activity. An HSV-1 mutant that does not express UL24 produced more viral R1 and R2 transcripts than the wild type or rescue virus relative to the amount of viral DNA. These results reveal a new role for HSV-1UL24 in regulating viral mRNA accumulation.