Lymphocyte proliferation and apoptosis of lymphocyte subpopulations in bovine leukemia virus-infected dairy cows with high and low proviral loa

NIETO FARIAS, MARIA VICTORIA; NOGUEIRA SOUZA FERNANDO; LENDEZ, PAMELA ANAHI; MARTINEZ CUESTA, LUCIA; REIS SANTOS KAMILA; DELLA LIBERA ALICE MELVILLE PAIVA; CERIANI MARIA CAROLINA; DOLCINI, GUILLERMINA LAURA

VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY

ELSEVIER SCIENCE BV

Lugar: Amsterdam; Año: 2018 vol. 206 p. 41 - 48

0165-2427

Bovine leukemia virus (BLV) is one of the most important virus in dairy cattle. The infection behavior followswhat we call the iceberg phenomenon: 60% of infected animals do not show clinical signs; 30% develop persistentlymphocytosis (PL); and the remaining 10%, die due to lymphosarcoma. BLV transmission depends oninfected cell exchange and thus, proviral load is determinant. Understanding the mechanisms by which cattlegoverns the control of viral dissemination will be desirable for designing effective therapeutic or preventivestrategies for BLV. The development of high proviral load (HPL) or low proviral load (LPL) might be associatedto genetic factors and humoral immune responses, however cellular responses are not fully described. It is knownthat BLV affects cellular homeostasis: proliferation and apoptosis. It is also known that the BLV tropism isdirected towards B lymphocytes, and that lymphocytotic animals have elevated amounts of these cells. Usually,when an animal is infected by BLV, the B markers that increase are CD21, CD5 and CD11b. This increase couldbe related to the modulation of apoptosis in these cells. This is the first work in which animals infected with BLVare classified according to their proviral load and the subpopulations of B and T lymphocytes are evaluated interms of their percentage in peripheral blood and its stage of apoptosis and viability. PBMCs from HPL animalsproliferated more than LPL and non-infected animals. CD11b+/CD5+ lymphocytes in LPL animals presentedgreater early and late apoptosis than HPL animals and cells of HPL animals had increased viability than LPLanimals. Our results confirm that BLV alters the mechanism of apoptosis and proliferation of infected cells.