The herpes simplex virus type 1 BgKL variant, unlike the BgOL variant, shows a higher association with orolabial infection than with infections at other sites, supporting the variant-dispersion-replacement hypothesis.

ABSTRACT

The identification and geographic distribution of the herpes simplex virus type 1 (HSV-1) BglII restriction fragment length polymorphism (RFLP) variants named BgK(L) and BgO(L) in clinical isolates from orolabial and cutaneous sites were described in our previous reports, in which the dispersion and replacement of HSV-1 variants were proposed. The base substitution sites deduced from the BgK(L) multiple RFLP variations were mapped to the U(L)12 (DNase), R(L)2 (alpha0 transactivator), and latency-associated transcript genes in the present study. The results show that the relative frequencies (RFs) of BgK(L) are significantly higher in orolabial and cutaneous HSV-1 infections than in ocular infections. For the BgO(L) variant, the opposite was found; i.e., the RF of BgO(L) was significantly lower in orolabial and cutaneous infections than in ocular infections. No significant differences in the RFs of non-BgK(L)non-BgO(L) isolates were observed. The ratio of the BgK(L) RF to the BgO(L) RF was much higher for the orolabial and cutaneous infection groups than for the ocular infection group, whereas the BgK(L) RF-to-non-BgK(L)non-BgO(L) RF ratios for the former groups were slightly higher than those for the latter group. The higher efficiency of orolabial and cutaneous infections caused by BgK(L) compared to the efficiency of infections caused by BgO(L) allows BgK(L) to spread more efficiently in human populations and to displace BgO(L), because the mouth and lips are the most common HSV-1 infection sites in children. The present study supports our HSV-1 dispersion-and-replacement hypothesis and suggests that HSV-1, the latency-reactivation of which allows variants to accumulate in human populations, has evolved under competitive conditions, providing a new perspective on the polymorphism or variation of HSV-1.