Correlation of cell surface marker expression with African swine fever virus infection

Abstract

The expression of surface markers on African swine fever virus (ASFV) infected cells was evaluated to assess their involvement in infection. Previous findings indicated CD163 expression was correlated with ASFV susceptibility. However, in this study the expression of porcine CD163 on cell lines did not increase the infection rate of these cells indicating other factors are likely to be important in determining susceptibility to infection. On adherent porcine bone marrow (pBM) cells the expression of CD45 was strongly correlated with infection. CD163 and CD203a expression correlated at intermediate levels with infection, indicating cells expressing these markers could become infected but were not preferentially infected by the virus. Most of the cells expressing MHCII were infected, indicating that they may be preferentially infected although expression of MHCII was not essential for infection and a large percentage of the infected cells were MHCII negative. CD16 showed a marked decrease in expression following infection and significantly lower levels of infected cells were shown to express CD16. Altogether these results suggest CD163 may be involved in ASFV infection but it may not be essential; the results also highlight the importance of other cell markers which requiring further investigation.

Phenotyping and susceptibility of established porcine cells lines to African Swine Fever Virus infection and viral production

“…Moreover, magnetically sorted CD163-positive blood monocytes were more susceptible to infection than monocytes lacking CD163, and the use of specific antibodies blocking the receptor resulted in different degrees of ASFV inhibition, suggesting that CD163 may be involved in the first steps of ASFV infection 43 . On the other hand, another study stated that CD163 is not needed for ASFV infection 44 and moreover, pigs lacking CD163 have been shown to be infected by Georgia 2007/1 ASFV 45 . This suggests that this receptor, although possibly involved in early steps in vitro , may not affect ASFV infection in vivo .…”

“…However, the susceptibility of host cells to ASFV seems to be linked to maturity since in vitro maturation of porcine blood monocyte cells (PBMCs) to macrophages, correlating with an up-regulation of CD203 and CD163 expression, has been shown to increase ASFV infection 24 , 43 . Nevertheless, the role of CD163 in ASFV infection is controversial since it has been published that the expression of CD163 alone is not enough to increase the susceptibility to the virus in non-permissive cells 44 , and pigs lacking CD163 showed no resistance to infection with the ASFV isolate Georgia 2007/1 45 .…”

Time course study of the response to LPS targeting the pig immune gene networks

“…The expression of porcine CD163 (a scavenger receptor belonging to a cysteine-rich superfamily) on monocytes/macrophages correlates with permissiveness to African swine fever infection [ 50 ]. CD163 is considered as the most important receptor for porcine reproductive and respiratory syndrome attachment and internalization [ 51 ].…”

Live attenuated African swine fever viruses as ideal tools to dissect the mechanisms involved in viral pathogenesis and immune protection

“…The up-regulation of CD163 has been associated with monocytes maturation into macrophages, and fits with the ability of ASFV to interact with the surface CD163 for viral entry [ 42 ]. The role of CD163 as receptor for ASFV entry has been proposed but not universally supported since reports demonstrated efficient infection of macrophages that do not express CD163 [ 44 ]. Regardless of this, the virus interaction with CD163 and other cell surface molecules most probably trigger the overexpression of the genes coding several pro-inflammatory cytokines: IL - 1β , IFN - γ , IL - 5 , IL - 6 , IL - 12p40 and TNF - α ; and also some anti-inflammatory mediators such as IL - 10 and TGF - βR1 that might contribute to controlling the first rounds of virus replication while avoiding harmful inflammation.…”