The microscopic findings of the present study suggested that lymphocytes located in the interfollicular region and mantle zone could be the primary targets for TTSuV; similarly, our previous study has demonstrated that both T and B lymphocytes are susceptible to PCV2 infection and PCV2 is capable of replicating in dividing lymphocytes (Lin et al., 2008). It has been shown that the replicating form of TTV could be detected in the peripheral blood mononuclear GSK690693 stimulated by phytohemagglutinin, lipopolysaccharide, and interleukin 2 (Mariscal et al., 2002). Furthermore, intracellular TTSuV signals could also be observed in large monocytoid cells or macrophages throughout the bone marrow, spleen, and other lymphoid tissues by ISH (Krakowka and Ellis, 2008 and Martin-Valls et al., 2008). Our previous study also showed that the PCV2-positive signals in the siLNs of wasting pigs were largely present in the monocyte/macrophage lineage cells with only scattered positive lymphocytes distributed in the germinal center or throughout the follicles (Lin et al., 2011). Considering the close similarity between PCV2 and TTSuV and the fact that PCV2 lacks of DNA polymerase, it is speculated that TTSuV may also replicate only in actively dividing cells by the use of host cell polymerase (Maggi et al., 2001 and Mariscal et al., 2002). Thus, activated lymphocytes will be an ideal place for TTSuV propagation. The presence of TTSuV in the monocytoid cells or macrophages in the lymphoid system might be a consequence of phagocytosis of TTSuV-infected lymphocytes; however, such assumption requires further elucidation.
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