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All six great ape species are listed as endangered or critically endangered by the IUCN and experiencing decreasing population trends. One of the threats to these non-human primates is the transmission of pathogens from humans. We conducted a literature review on occurrences of pathogen transmission from humans to great apes to highlight this often underappreciated issue. In total, we found 33 individual occurrences of probable or confirmed pathogen transmission from humans to great apes: 23 involved both pathogen and disease transmission, 7 pathogen transmission only, 2 positive antibody titers to zoonotic pathogens, and 1 pathogen transmission with probable disease. Great ape populations were categorized into captive, semi-free-living, and free-living conditions. The majority of occurrences involved chimpanzees (Pan troglodytes) (n = 23) or mountain gorillas (Gorilla beringei beringei) (n = 8). These findings have implications for conservation efforts and management of endangered great ape populations. Future efforts should focus on monitoring and addressing zoonotic pathogen and disease transmission between humans, great ape species, and other taxa to ensure the health of humans, wild and domestic animals, and the ecosystems we share.

Careful studies of mouse trigeminal ganglia (TG) latently infected with herpes simplex virus type 1 (HSV-1) indicate the presence of productive cycle viral gene products and persistent immune response, suggesting ongoing spontaneous viral reactivation in these tissues. In the present study we set out to determine whether infectious virus is present in murine TG latently infected with HSV-1 (KOS). At 37 days after ocular inoculation we found a small amount of infectious virus in ca. 6% of latently infected murine TG. Furthermore, the amount of infectious virus that we detected (PFU per viral antigen-positive neuron) was similar to that detected in acutely infected ganglia. We conclude that spontaneous reactivation of infectious HSV-1 occurs in the mouse TG and is likely the principle cause of viral protein expression in these tissues. We next examined the role of latency-associated transcript (LAT) in spontaneous ganglionic reactivation by examining ganglia latently infected with KOS dlLAT1.8, a LAT deletion virus. Through the use of immunocytochemistry we found that KOS dlLAT1.8 had a rate of spontaneous ganglionic reactivation very similar to that of HSV-1 (KOS). Studying spontaneous ganglionic reactivation of HSV in the mouse TG allows a direct study of viral reactivation from latently infected neurons without the potential confounders and complicating downstream events that accompany the study of viral reactivation by explantation or peripheral viral shedding. Since most cases of human viral shedding and reactivation are not associated with a known trigger, spontaneous ganglionic reactivation of HSV-1 may be a better model of human disease than existing models.

We previously demonstrated that herpes simplex virus type 1 (HSV-1) preferentially establishes latent infection in monoclonal antibody (MAb) A5-positive ganglionic neurons and that a 2.8-kb portion of the HSV-1 genome, corresponding to the 5 end of the LAT (latency-associated transcript) coding region, is responsible for this phenotype (38, 65). In the current study we carried out further genetic mapping of this latency phenotype and investigated some of the mechanisms that might be responsible. Studies with the chimeric virus HSV-1 17syn؉/LAT2, an HSV-1 virus engineered to express HSV-2 LAT, demonstrated that this virus exhibited an HSV-2 latency phenotype, preferentially establishing latency in MAb KH10-positive neurons. This result is complementary to that previously described for the chimeric virus HSV-2 333/LAT1 and indicate that the HSV-1 latency phenotype can be changed to that of HSV-2 by substitution of a 2. Primary infection with herpes simplex virus (HSV) is characterized by local viral replication at the site of inoculation as well as retrograde axonal transport of the virus to regional sensory ganglia where a latent infection may be established. Sensory ganglia are comprised of a heterogeneous population of neurons, and work in our laboratory has demonstrated that different subpopulations of murine ganglionic neurons have different outcomes of infection with HSV (38,39,65). Of the subpopulations of ganglionic neurons that we have studied, those neurons recognized by monoclonal antibodies (MAbs) A5 (specific for a population of neurons expressing Gal␤1-4GlcNAc-R epitopes) and KH10 (specific for a different population of ganglionic neurons expressing Gal␣1-3Gal␤1-4NAc-R epitopes) have the most distinct susceptibility phenotypes (19,22,65). Although all neuronal subpopulations appear to be capable of supporting a productive infection with either HSV type 1 (HSV-1) or HSV-2, as assayed by in situ hybridization for the latency-associated transcripts (LAT), HSV-1 preferentially establishes a latent infection in A5-positive neurons whereas HSV-2 preferentially establishes a latent infection in KH10-positive neurons (38), a pattern that is observed following both ocular and footpad inoculation.In the mouse trigeminal ganglion (TG) MAbs A5 and KH10 recognize functionally distinct neuronal populations. Most A5-positive neurons are immunoreactive for neuropeptides and the high affinity nerve growth factor receptor (and terminate in lamina I and IIa of the dorsal horn of the spinal cord), whereas KH10-positive neurons colabel with the lectin BSL-IB 4 (Bandeiraea simplicifolia isolectin B 4 ), identifying them as a population of small-diameter, peripherin-positive, glial cell line-derived neurotrophic factor-responsive, but vanilloid receptor-negative neurons that terminate largely in lamina IIb of the dorsal horn of the spinal cord (3,19,38,42,52,67). These observations highlight the importance of studying the interaction of HSV with different sensory neuronal subtypes in order to gain a complete understanding ...