VARV-CrmB is a TNF binding protein of variola virus. VARV-CrmB protein was previously
shown to be active as a TNF-antagonist in a number of in vivo and in vitro models. Here we investigated
the epicutaneous effect of recombinant VARV-CrmB protein using an experimental model of muTNFinduced
migration of skin leukocytes as well as colony forming activity of bone marrow cells (BMC).
Epiсutaneous applications of muTNF enhanced the number of cells migrating from skin flaps of BALB/c
mice, whereas subsequent applications of VARV-CrmB protein in 30 min after muTNF, abolished that effect. Epicutaneously
applied muTNF influenced the activity of committed hematopoietic progenitors causing a reduction of erythroid
(BFUe+CFUe) colonies and increase of granulocyte-macrophage (CFU-GM) colonies in the colony-forming tests.
VARV-CrmB, applied in combination with muTNF, demonstrated an ability to reverse this effect, namely, to increase
BFUe+CFUe and reduce CFU-GM back to the control levels. Taking together, these data demonstrate the TNF-blocking
properties of VARV-CrmB in vivo at epicutaneous applications. As effective TNF antagonist VARV-CrmB protein might
be conceded as a beneficial candidate for future research and development of therapeutic approaches in the field of inflammatory
Keywords: Cell migration, hematopoiesis, murine TNF (muTNF), tumor necrosis factor alpha (TNF), TNF-binding protein of
variola virus (VARV-CrmB).
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