The Synergy of Chicken Anemia Virus and Gyrovirus Homsa 1 in Chickens

Abstract

Chicken anemia virus (CAV) and Gyrovirus homsa 1 (GyH1) are members of the Gyrovirus genus. The two viruses cause similar clinical manifestations in chickens, aplastic anemia and immunosuppression. Our previous investigation displays that CAV and GyH1 often co-infect chickens. However, whether they have synergistic pathogenicity in chickens remains elusive. Here, we established a co-infection model of CAV and GyH1 in specific pathogen-free (SPF) chickens to explore the synergy between CAV and GyH1. We discovered that CAV and GyH1 significantly inhibited weight gain, increased mortality, and hindered erythropoiesis in co-infected chickens. Co-infected chickens exhibited severe immune organ atrophy and lymphocyte exhaustion. The proventriculus and gizzard had severe hemorrhagic necrosis and inflammation. We also discovered that the viral loads and shedding levels were higher and lasted longer in CAV and GyH1 co-infected chickens than in mono-infected chickens. Our results demonstrate that CAV and GyH1 synergistically promote immunosuppression, pathogenicity, and viral replication in co-infected chicken, highlighting the interaction between CAV and GyH1 in the disease process and increasing potential health risk in the poultry breeding industry, and needs further attention.

Development of a DAS–ELISA for Gyrovirus Homsa1 Prevalence Survey in Chickens and Wild Birds in China

“…In particular, GyH1 mono-infection experiments showed that GyH1 virus shedding began at 14 days post-infection, peaked at 21 days post-infection, and began to decrease at 28 days post-infection. Additionally, immune organ dynamic monitoring experiments and erythrocyte testing experiments have further validated our results [14,15,19].…”

“…Co–infection of GyH1 with other gyroviruses, e.g., gyrovirus galga1 (GyG1) and CAV, occurs frequently. Importantly, GyH1 co–infection with CAV leads to higher mortality and more widespread lymphocyte apoptosis [ 19 ], which increases the risk posed and makes prevention and control more difficult. Specifically, epidemiology investigation suggests that GyH1 is widespread in China, which is consistent with our findings [ 17 , 18 , 20 ].…”

“…Furthermore, GyH1 consists of three major proteins, the capsid protein VP1, the backbone protein VP2, and the apoptosis protein VP3. The VP1 protein plays an important role in viral virulence, replication, and infection of host cells [ 14 , 19 ]. For this reason, we prepared a series of anti–GyH1 monoclonal antibodies based on a highly antigenic and conserved fragment of the VP1 protein.…”

“…The highest positive rate present in chickens between 14 and 35 days of age indicates that GyH1 is self–limited. In our previous in vivo experiment, we noticed that infection with GyH1 in the early life of chickens triggers massive apoptosis of hematoblasts, promyeloblasts, and lymphocytes in the bone marrow, resulting in a rapid proliferation of GyH1 in a short period and a rapid increase in viral titers in the blood [ 14 , 19 ]. Subsequently, virus load in the blood decreases with age due to lymphocyte and promyelocyte regeneration and hematopoietic cell activity recovery.…”

Prevalence and phylogenetic analysis of Gyrovirus galga 1 in southern China from 2020 to 2022

“…In recent years, other circoviruses have been reported, and several species have been shown to be pathogenic to poultry ( Truchado et al, 2019 ; Feher et al, 2022 ; Yan et al, 2023 ). Yang et al found that GyH1 and CAV synergistically promote immunosuppression, pathogenicity, and viral replication in co-infected chicken, highlighting the interaction between CAV and GyH1 in the disease process and increasing potential health risk in the poultry breeding industry ( Yang et al, 2023 ). As an early discovered and reported avian gyroviruses, GyVg1 should draw more attention to its public health and safety hazards, and as a member of the gyroviruses, GyVg1 also provides valuable research materials for human studies to reveal the life cycle of gyroviruses.…”