| Autor: |
Avagyan H; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia.; Experimental Laboratory, Yerevan State Medical University after M. Heratsy, Yerevan 0025, Armenia., Hakobyan S; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia., Baghdasaryan B; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia., Arzumanyan H; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia., Poghosyan A; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia., Bayramyan N; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia., Semerjyan A; Department of Medical Biology and Genetics, Yerevan State Medical University after M. Heratsy, Yerevan 0025, Armenia., Sargsyan M; Department of Epizootiology and Parasitology, Armenian National Agrarian University, Yerevan 0009, Armenia., Voskanyan H; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia., Vardanyan T; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia., Karalyan N; Department of Pathological Anatomy and Clinical Morphology, Yerevan State Medical University after M. Heratsi, Yerevan 0025, Armenia., Hakobyan L; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia., Abroyan L; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia., Avetisyan A; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia.; Experimental Laboratory, Yerevan State Medical University after M. Heratsy, Yerevan 0025, Armenia., Karalova E; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia.; Experimental Laboratory, Yerevan State Medical University after M. Heratsy, Yerevan 0025, Armenia., Semerjyan Z; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia.; Experimental Laboratory, Yerevan State Medical University after M. Heratsy, Yerevan 0025, Armenia., Karalyan Z; Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia.; Department of Medical Biology and Genetics, Yerevan State Medical University after M. Heratsy, Yerevan 0025, Armenia. |
| Abstrakt: |
Shortly after the establishment of African swine fever virus (ASFV) genotype II in 2007, cases of acute fatal infection were observed. However, after several years of circulation in the Eurasian region, the clinical signs of the disease changed. Currently, this disease can occur acutely, subclinically, chronically, or asymptomatically. Cases of the complete recovery of infected pigs, and the disappearance of ASFV from their tissues and secretions have been described. This form of the disease first appeared in Armenia at the end of 2011. This virus was described and identified as the Dilijan2011IMB strain. The goal of our research was to study the main features of clinical, pathological, immunological, virological, and genetic parameters involved in the development of new forms of African swine fever (ASF). Chronic ASF was characterized with low titers of the virus and a decrease in the intensity of hemadsorption. Additionally, a reduced intensity in clinical symptoms and pathoanatomical results was noted. The absolute, but not the relative number of immune cells changes; the neutropenia (in bone marrow and spleen), lymphopenia (in bone marrow), lymphocytosis (only in spleen), lymphoid cell depletion (in bone marrow), and pancytopenia (in bone marrow) observed in the chronic form of ASF were less pronounced compared to in the acute form. When comparing the late stage of chronic ASF to the acute form, the key cytological indicators in the spleen, lymph nodes, and blood were less severe in the chronic stage. Bone marrow failure in the chronic form, expressed in a pronounced decrease in all cell types, generally coincided with the data in the acute form of ASF. The same data were obtained after assessing serum TNF-alpha levels. Thus, we can conclude that the chronic form of ASF occurs due to a less pronounced immune response, as well as a decrease in virus titers in the blood and tissues of infected pigs. |
