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Clinical symptoms
Infection with ALV can lead to tumor formation, especially lymphoid leukosis, primarily in the liver, spleen, and bursa. Tumors may also occasionally develop in the kidneys and reproductive organs. The characteristics and frequency of these tumors are influenced by factors such as the virus strain, chicken breed, age, and transmission route.
Common clinical signs include:
- loss of appetite
- weakness
- diarrhea
- dehydration
- weight loss
- depression
- enlarged bursa and sometimes an enlarged liver
Infected birds may also lay fewer eggs, and while they may not necessarily develop tumors, these symptoms may still be present.
Host immune response against ALV
The host's immune response to ALV begins with the innate immune system, the first line of defense against pathogens. However, ALV has been shown to suppress the host's innate immune response.
- Monocytes are precursor cells for macrophages and dendritic cells (DCs), both of which are essential for innate and adaptive immunity.
- Macrophages play a critical role in innate immunity by clearing pathogens, regulating immune responses, and maintaining tissue integrity through the secretion of pro-inflammatory cytokines when activated by viruses, microbes, or cytokines.
- DCs, as sentinel cells, are key in pathogen recognition, antigen presentation, and T-cell stimulation. In ALV-J-infected bone marrow-derived dendritic cells (BM-DCs), differentiation and maturation are significantly inhibited, resulting in apoptosis due to the abnormal expression of microRNAs.
Diagnosis
Standard criteria include evaluating the patient's history, clinical signs, gross pathological findings, and conducting histological examinations.
In more advanced cases, additional methods such as immunohistochemical testing, standard and quantitative PCR assays, virus isolation, and serological testing are employed.