The giant panda (Ailuropoda melanoleuca) is a vulnerable mammal herbivore living wild in central China. Viral infections have become a potential threat to the health of these endangered animals, but limited information related to these infections is available. Using a viral metagenomic approach, we surveyed viruses in the feces, nasopharyngeal secretions, blood, and different tissues from a wild giant panda that died from an unknown disease, a healthy wild giant panda, and 46 healthy captive animals. The previously uncharacterized complete or near complete genomes of four viruses from three genera in Papillomaviridae family, six viruses in a proposed new Picornaviridae genus (Aimelvirus), two unclassified viruses related to posaviruses in Picornavirales order, 19 anelloviruses in four different clades of Anelloviridae family, four putative circoviruses, and 15 viruses belonging to the recently described Genomoviridae family were sequenced. Reflecting the diet of giant pandas, numerous insect virus sequences related to the families Iflaviridae, Dicistroviridae, Iridoviridae, Baculoviridae, Polydnaviridae, and subfamily Densovirinae and plant viruses sequences related to the families Tombusviridae, Partitiviridae, Secoviridae, Geminiviridae, Luteoviridae, Virgaviridae, and Rhabdoviridae; genus Umbravirus, Alphaflexiviridae, and Phycodnaviridae were also detected in fecal samples. A small number of insect virus sequences were also detected in the nasopharyngeal secretions of healthy giant pandas and lung tissues from the dead wild giant panda. Although the viral families present in the sick giant panda were also detected in the healthy ones, a higher proportion of papillomaviruses, picornaviruses, and anelloviruses reads were detected in the diseased panda. This viral survey increases our understanding of eukaryotic viruses in giant pandas and provides a baseline for comparison to viruses detected in future infectious disease outbreaks. The similar viral families detected in sick and healthy giant pandas indicate that these viruses result in commensal infections in most immuno-competent animals.

Several animal species can reportedly act as reservoirs for Hepatitis E virus (HEV), a zoonotic pathogen. HEV and antibody to the virus have been detected in a variety of animals including rodents. Pig and rat models for HEV have been established for HEV, but a nude mouse has not yet been developed.

The crosstalk between the gut microbiota and immune state of the host is an essential focus in academia and clinics. To explore the dynamic role of the microbiota in response to immune deficiency, we comprehensively assessed the microbiome of 90 mouse fecal samples, across three time points including two immunodeficiency models, namely severe combined immunodeficient (SCID) mice and non-obese diabetic SCID (NOD/SCID) mice, with BALB/cA as a control strain. Metagenomic analysis revealed a decrease in alpha diversity and the existence of a clear structural separation in the microbiota of immunodeficient mice. Although nuances exist between SCID and NOD/SCID mice, an increase in the protective microbiota, in particular Lactobacillus, contributed the most to the discrimination of immunodeficient and control mice. Further data regarding the red blood cell (RBC) concentration and serum IgA level during different stages of development support the concept of the microbiota alleviating the advancement of immune deficiency, which is called microbial compensation. Taken together, these results demonstrate the dynamic impact of immunodeficiency on the gut microbiota and the adaptive alteration of the microbiota that may influence the host state.