Mountain gorilla lymphocryptovirus has Epstein-Barr virus-like epidemiology and pathology in infants

Epstein-Barr virus (EBV) infects greater than 90% of humans, is recognized as a significant comorbidity with HIV/AIDS, and is an etiologic agent for some human cancers. The critically endangered mountain gorilla population was suspected of infection with an EBV-like virus based on serology and infant histopathology similar to pulmonary reactive lymphoid hyperplasia (PRLH), a condition associated with EBV in HIV-infected children. To further examine the presence of EBV or an EBV-like virus in mountain gorillas, we conducted the first population-wide survey of oral samples for an EBV-like virus in a nonhuman great ape. We discovered that mountain gorillas are widely infected (n = 143/332) with a specific strain of lymphocryptovirus 1 (GbbLCV-1). Fifty-two percent of infant mountain gorillas were orally shedding GbbLCV-1, suggesting primary infection during this stage of life, similar to what is seen in humans in less developed countries. We then identified GbbLCV-1 in post-mortem infant lung tissues demonstrating histopathological lesions consistent with PRLH, suggesting primary infection with GbbLCV-1 is associated with PRLH in infants. Together, our findings demonstrate that mountain gorilla's infection with GbbLCV-1 could provide valuable information for human disease in a natural great ape setting and have potential conservation implications in this critically endangered species

Brain development and perinatal vulnerability to cerebral damage

The recent exponential rise in detailed magnetic resonance (MR) imaging studies has emphasized the concept of gestationally determined regional vulnerability in the brain: the site and nature of the injury sustained being determined by a combination of the characteristics of the insult, the specific tissue and cell vulnerability and the gestation of the infant. The type of insult may also be partly dependent on gestation. However, it is now known that acute perinatal hypoxic ischemic events, previously considered characteristic for the term born neonate presenting with hypoxic-ischemic encephalopathy (HIE), may occur at earlier points in gestation [1, 2]. Nevertheless, such events occur less often in the infant born preterm where lesions develop in similar brain regions and in other areas characteristically more vulnerable in more premature babies (Fig. 127.1). Similarly, white matter (WM) lesions, which are considered the hallmark of injury to the preterm brain because they are characteristic of perinatal injury relating to inflammation, infection or hypoglycemia in the term brain, may also occur in a small percentage of neonates with an encephalopathy (Fig. 127.2) [3]