The human–primate interface in the New Normal: Challenges and opportunities for primatologists in the COVID-19 era and beyond

The emergence of SARS-CoV-2 in late 2019 and human responses to the resulting COVID-19 pandemic in early 2020 have rapidly changed many aspects of human behavior, including our interactions with wildlife. In this commentary, we identify challenges and opportunities at human–primate interfaces in light of COVID-19, focusing on examples from Asia, and make recommendations for researchers working with wild primates to reduce zoonosis risk and leverage research opportunities. First, we briefly review the evidence for zoonotic origins of SARS-CoV-2 and discuss risks of zoonosis at the human–primate interface. We then identify challenges that the pandemic has caused for primates, including reduced nutrition, increased intraspecific competition, and increased poaching risk, as well as challenges facing primatologists, including lost research opportunities. Subsequently, we highlight opportunities arising from pandemic-related lockdowns and public health messaging, including opportunities to reduce the intensity of problematic human–primate interfaces, opportunities to reduce the risk of zoonosis between humans and primates, opportunities to reduce legal and illegal trade in primates, new opportunities for research on human–primate interfaces, and opportunities for community education. Finally, we recommend specific actions that primatologists should take to reduce contact and aggression between humans and primates, to reduce demand for primates as pets, to reduce risks of zoonosis in the context of field research, and to improve understanding of human–primate interfaces. Reducing the risk of zoonosis and promoting the well-being of humans and primates at our interfaces will require substantial changes from “business as usual.” We encourage primatologists to help lead the way.     

Development and evolution of the tetrapod skull–neck boundary

The origin and evolution of the vertebrate skull have been topics of intense study for more than two centuries. Whereas early theories of skull origin, such as the influential vertebral theory, have been largely refuted with respect to the anterior (pre‐otic) region of the skull, the posterior (post‐otic) region is known to be derived from the anteriormost paraxial segments, i.e. the somites. Here we review the morphology and development of the occiput in both living and extinct tetrapods, taking into account revised knowledge of skull development by augmenting historical accounts with recent data. When occipital composition is evaluated relative to its position along the neural axis, and specifically to the hypoglossal nerve complex, much of the apparent interspecific variation in the location of the skull–neck boundary stabilizes in a phylogenetically informative way. Based on this criterion, three distinct conditions are identified in (i) frogs, (ii) salamanders and caecilians, and (iii) amniotes. The position of the posteriormost occipital segment relative to the hypoglossal nerve is key to understanding the evolution of the posterior limit of the skull. By using cranial foramina as osteological proxies of the hypoglossal nerve, a survey of fossil taxa reveals the amniote condition to be present at the base of Tetrapoda. This result challenges traditional theories of cranial evolution, which posit translocation of the occiput to a more posterior location in amniotes relative to lissamphibians (frogs, salamanders, caecilians), and instead supports the largely overlooked hypothesis that the reduced occiput in lissamphibians is secondarily derived. Recent advances in our understanding of the genetic basis of axial patterning and its regulation in amniotes support the hypothesis that the lissamphibian occipital form may have arisen as the product of a homeotic shift in segment fate from an amniote‐like condition.     

Early host–microbe interaction in a peri‐implant oral mucosa‐biofilm model

The host‐microbe relationship is pivotal for oral health as well as for peri‐implant diseases. Peri‐implant mucosa and commensal biofilm play important roles in the maintenance of host‐microbe homeostasis, but little is known about how they interact. We have therefore investigated the early host‐microbe interaction between commensal multispecies biofilm (Streptococcus oralis, Actinomyces naeslundii, Veillonella dispar, Porphyromonas gingivalis) and organotypic peri‐implant mucosa using our three‐dimensional model. After 24 hr, biofilms induced weak inflammatory reaction in the peri‐implant mucosa by upregulation of five genes related to immune response and increased secretion of IL‐6 and CCL20. Biofilm volume was reduced which might be explained by secretion of β‐Defensins‐1, ‐2, and CCL20. The specific tissue reaction without intrinsic overreaction might contribute to intact mucosa. Thus, a relationship similar to homeostasis and oral health was established within the first 24 hr. In contrast, the mucosa was damaged and the bacterial distribution was altered after 48 hr. These were accompanied by an enhanced immune response with upregulation of additional inflammatory‐related genes and increased cytokine secretion. Thus, the homeostasis‐like relationship was disrupted. Such profound knowledge of the host‐microbe interaction at the peri‐implant site may provide the basis to improve strategies for prevention and therapy of peri‐implant diseases.     

Precipitation patterns and N availability alter plant-soil microbial C and N dynamics

Plant and Soil - Contrasting nutrient-acquisition strategies would explain why species differ in their distribution in relation to soil phosphorus (P) availability, promoting diversity. However,...     

Antimicrobial resistance patterns among different Escherichia coli isolates in the Kingdom of Saudi Arabia

Antimicrobial resistance patterns among different Escherichia coli isolates in the Kingdom of Saudi Arabia. This study aimed to investigate the patterns of antimicrobial resistance in E. coli isolated from different samples, and to identify potential pathogenic isolates in Riyadh, Kingdom of Saudi Arabia (KSA). In total, 51 bacterial isolates were recovered from 113 samples of human urine, food (raw meat, raw chicken, raw egg surface, and fresh vegetables), water, and air. Twenty-four E. coli isolates were tested for susceptibility to 26 antibiotics. The air sample isolates were most resistant to amoxicillin, ampicillin, amoxicillin/clavulanic acid, amoxicillin/sulbactam, piperacillin/tazobactam, cefalotin, cefuroxime, cefoxitin, cefixime, nitrofurantoin, and trimethoprim/sulfamethoxazol. The isolates from vegetable samples were resistant to amoxicillin, ampicillin, amoxicillin/clavulanic acid, amoxicillin/sulbactam, cefalotin, cefuroxime, cefoxitin, and cefixime. By contrast, the isolates from the water samples were resistant only to amoxicillin and ampicillin. The isolates from the human urine samples were most frequently resistant to norfloxacin (80%) followed by amoxicillin and ampicillin (70%), trimethoprim/sulfamethoxazole (55%), ciprofloxacin and ofloxacin (50%), cefalotin (30%), cefuroxime, cefixime and cefotaxime (25%), ceftazidime, ceftriaxone, cefepime and aztreonam (20%), amoxicillin/clavulanic acid, piperacillin/tazobactam and gentamicin (10%), and amoxicillin/sulbactam and cefoxitin (5%). Almost all (23/25, 95.8%) (n = 23) of the isolates were multi-drug resistant (MDR) (i.e., resistant to 3 or more classes of antibiotics), and 16.7% (n = 4) of those were positive for extended spectrum β-lactamase (ESBL). Of the 4 ESBL-producers, 3 were positive for blaCTX_-M-15 and blaCTX_-M1_group, 2 were positive for blaCMY_-2, and 1 each was positive for blaCTX_{-M-2 group,} blaSHV, and blaOXA_-47. The quinolone resistance gene qnrS was detected in 25% (n = 6) of the E. coli strains isolated from urine (N = 5) and air (N = 1) samples. The considerable number of antimicrobial resistance genes detected among E. coli isolates tested here is alarming and should raise public health concern.     

Differential effects of cysteine and methionine residues in the antioxidant activity of human serum albumin

Antioxidant properties of human serum albumin (HSA) may explain part of its beneficial role in various diseases related to free radical attack. In the present study, the antioxidant role of Cys and Met was studied by copper-mediated oxidation of human low density lipoproteins and by free radical-induced blood hemolysis which essentially assessed metal-chelating and free radical scavenging activities, respectively. Mild conditions were set up to specifically modify Cys and Met residues by N-ethylmaleimide (NEM) and chloramine T treatments, respectively. We found that Met and Cys accounted for 40–80% of total antioxidant activity of HSA. Copper binding to HSA was decreased by about 50% with chloramine T treatment of Met whereas no change was observed after NEM treatment of Cys. Although other amino acid residues are likely to be involved in anti-/prooxidant properties of HSA, from our data, we propose that Cys chiefly works as a free radical scavenger whereas Met mainly acts as a metal chelator.     

Co-regulation of senescence-associated genes by oncogenic homeobox proteins and polycomb repressive complexes

Cellular senescence is a stable cell cycle arrest that can be induced by stresses such as telomere shortening, oncogene activation or DNA damage. Senescence is a potent anticancer barrier that needs to be circumvented during tumorigenesis. The cell cycle regulator p16^INK4a is a key effector upregulated during senescence. Polycomb repressive complexes (PRCs) play a crucial role in silencing the INK4/ARF locus, which encodes for p16^INK4a, but the mechanisms by which PRCs are recruited to this locus as well as to other targets remain poorly understood. Recently we discovered the ability of the homeobox proteins HLX1 (H2.0-like homeobox 1) and HOXA9 (Homeobox A9) to bypass senescence. We showed that HLX1 and HOXA9 recruit PRCs to repress INK4a, which constitutes a key mechanism explaining their effects on senescence. Here we provide evidence for the regulation of additional senescence-associated PRC target genes by HLX1 and HOXA9. As both HLX1 and HOXA9 are oncogenes implicated in leukemogenesis, we discuss the implications that the collaboration between Homeobox proteins and PRCs has for senescence and cancer.