Anemia Virus Infection Research Articles

Serologically silent, occult equine infectious anemia virus (EIAV) infections in horses

Serologically silent, occult equine infectious anemia virus (EIAV) infections in horses

Lessons in AIDS Vaccine Development Learned from Studies of Equine Infectious, Anemia Virus Infection and Immunity

Equine infectious anemia (EIA), identified in 1843 [1] as an infectious disease of horses and as a viral infection in 1904, remains a concern in veterinary medicine today. Equine infectious anemia virus (EIAV) has served as an animal model of HIV-1/AIDS research since the original identification of HIV. Similar to other lentiviruses, EIAV has a high propensity for genomic sequence and antigenic variation, principally in its envelope (Env) proteins. However, EIAV possesses a unique and dynamic disease presentation that has facilitated comprehensive analyses of the interactions between the evolving virus population, progressive host immune responses, and the definition of viral and host correlates of immune control and vaccine efficacy. Summarized here are key findings in EIAV that have provided important lessons toward understanding long term immune control of lentivirus infections and the parameters for development of an enduring broadly protective AIDS vaccine.

Dynamics of equine infectious anemia virus (EIAV) infection in naturally infected mules

African horse sickness (AHS) is a severe, non-contagious, insect-borne disease that causes high mortality in horses. Little information is available on the effects of AHS on clinical parameters. The objective of this study was to evaluate the cardiac system to aid on treatment and prognosis of AHS. Horses hospitalized at the Onderstepoort Veterinary Academic Hospital with confirmed AHS were included in the study after owner’s consent. Physical examination, base-apex ECG, echocardiography and serum cardiac troponin I (cTnI) were evaluated at different times until horses were either discharged or euthanized. A total of 11 horses were included, 6 survived and 5 were euthanized. Mean (range) heart rate at arrival was 59 (42-76) beats per minute. Tachycardia was present in 81% of the horses at arrival, 5/6 horses at discharge and in 4/5 horses at the time of euthanasia. cTnI was elevated at arrival in 2/6 survivors and 4/5 of the euthanized horses; however it increased above normal values (>0.03 ng/ml) in 10/11 horses as the disease progressed. Electrocardiography and echocardiography were normal in all horses at all times. This is the first report of cardiac evaluation in horses with AHS. Tachycardia and myocardial damage were common findings even at discharge. Serial cTnI measurements may be useful to evaluate disease progression and prognosis. cTnI needs to be evaluated before return to exercise is considered. Drugs that may affect the cardiac system function should be avoided. Abnormalities were not detected by ECG or echocardiography even when performed frequently.

Chicken infectious anaemia vaccinal strain persists in the spleen and thymus of young chicks and induces thymic lymphoid cell disorders

The chicken infectious anaemia virus (CIAV) infection may induce immunosuppression and persistent infection. The use of vaccination in young chicks is still controversial due to its low immune efficiency. In order to verify the viral persistency of a vaccinal strain of CIAV and its associated-lymphoid cell disorders, 54 1-day-old specific pathogen free chicks were vaccinated (CIAV-VAC®; Intervet, Millsboro, Delaware, USA) and haematologic examination, expression of viral VP3 gene, humoral response and phenotyping of lymphoid cells were studied in lymphoid organs at various times post vaccination (p.v.). No clinical signs were observed but light heteropaenia was detected in CIAV-vaccinated chicks. The VP3 gene of CIAV was detected by polymerase chain reaction in the thymus and spleen from day 7 until 28 days p.v. Thymic larger CD4+CD8+ cells increased only at 7 days p.v. while smaller CD4+CD8+ cells decreased after 14 and 28 days in CIAV-vaccinated birds. The CD4 expression, in contrast to that seen for CD8, decreased in thymocytes from the CIAV-vaccinated group. In the spleen and bursa, the percentage of CD8+ cells increased at 7 and 28 days p.v. only, while CD4+ cells decreased simultaneously. The vaccinated chicks also exhibited a higher number of splenic CD3–CD8+ cells (natural killer cells). The anti-CIAV antibody responses, however, remained low in most vaccinated chicks and did not persist up to 18 days p.v. These results suggest that the vaccinal virus strain is clinically attenuated but persists in the thymus and spleen in some birds, inducing a low humoral immune response and altering thymopoiesis.

Viral load in 1-day-old and 6-week-old chickens infected with chicken anaemia virus by the intraocular route

Although the effects of chicken anaemia virus (CAV) infection have frequently been investigated in young chickens, there have been few studies of the pathogenesis of CAV infection in older birds. The aim of the work reported here was to study viral loads in 6-week-old chickens and to compare these with those seen in younger birds. Specific pathogen free chickens were inoculated at 1 day or at 6 weeks of age with 10(4) median tissue culture infective doses of CAV by the intraocular route. Chicks infected when 1 day old were euthanized at day 14, 18 or 22 post inoculation (p.i.), and those infected when 6 weeks old at day 16, 18 or 20 p.i. Their body and thymus weights were determined and samples were collected from their spleen, liver and thymus. A quantitative polymerase chain reaction assay was developed and used to determine the number of viral genome copies in the tissue samples. In both age groups, viral genome concentrations increased in all organs up to day 18 p.i. and reached a peak in the spleen and liver at day 18 p.i. The peak viral concentrations in the thymus were detected at day 18 in the younger birds and at day 20 p.i. in older chickens. These studies have shown that exposure to CAV in older birds leads to similar levels of active viral replication to those seen in younger birds, and may result in subclinical infections in older birds with the potential to increase susceptibility to other infectious agents.

Leukocyte-reduced red blood cell transfusions in patients with anemia and human immunodeficiency virus infection: The viral activation transfusion study: A randomized controlled trial

Leukocyte-reduced red blood cell transfusions in patients with anemia and human immunodeficiency virus infection: The viral activation transfusion study: A randomized controlled trial

Interaction of chicken anaemia virus and Cryptosporidium baileyi in experimentally infected chickens

The natural occurrence of concomitant chicken anaemia virus (CAV) and Cryptosporidium baileyi infection was described earlier. In this experiment, 1-day-old chickens were infected with CAV alone (anaemia virus infected, AI) or followed by inoculation with 8×10 5 C. baileyi oocysts orally at 1 wk of age (anaemia virus and Cryptosporidium infected, ACI). Another group of chickens received the same dose of C. baileyi oocysts without previous virus infection ( Cryptosporidium infected, CI), and two groups of uninfected chickens served as controls. Except one group (uninfected control, UC), all groups — including the other control group (challenged control, CC) — were challenged with an oral inoculum of 8×10 5 C. baileyi oocysts at the age of 4 wk. Haematological, serological, immunohistochemical and pathological findings confirmed the effect of the virus agent. The individual C. baileyi oocyst shedding did not show significant difference between group CI and ACI, however, after challenge infection the AI chickens shed approximately three times more C. baileyi oocysts than those in group CC. Mortality and the percentage of birds that developed anaemia was significantly higher among ACI than AI chickens, while haematocrit values at 2 wk of age and relative bursal weights at 4 wk of age were moderately lower in the ACI group. The results presented here suggest that concurrent CAV infection increases the reproductive potential of C. baileyi in chickens, and both pathogens have synergistic effect on each other.