P-463. Diversity of KSHV Subtypes in People Living with HIV in a Large Urban Center in Dallas, Texas

Abstract Background Human herpesvirus-8 (HHV-8), also known as Kaposi’s sarcoma-associated herpesvirus (KSHV), causes Kaposi’s sarcoma (KS) and other KSHV-associated disease (KAD). We previously described high KSHV seroprevalence and high KS incidence in a population of men who have sex with men (MSM) with HIV in Dallas, Texas. We now describe viral genetics in the same population.Table 1:Participant Characteristics Methods We analyzed samples from participants recruited in 2 different studies, one enrolling MSM with HIV with and without KAD, and the other enrolling MSM with HIV and KAD. We measured KSHV IgG in serum using a combination of ELISA and a bead-based multiplex assay. Oral fluid samples of all individuals with KAD and seropositive individuals with no KAD were analyzed by RT-PCR to detect and quantify KSHV DNA. Samples with detectable KSHV underwent Sanger and/or next generation sequencing to determine K1 subtype.Figure 1:Phylogenetic Tree of Participant Samples Results Overall, 281 participants were recruited; 59 shed enough virus for K1 subtyping. Of these, 37 did not have KAD, and 22 had KAD, all had KS. Table 1 describes the demographic characteristics of these participants. Notably, those with KS had lower median CD4 countsthan those without KS (p < 0.01). All known K1 subtypes, except for D, were identified in this cohort, including the rare E and F subtypes. The latter, which only recently had been described outside Africa was identified in 6 individuals. Four participants had mixed infections with 2 or more KSHV subtype (Figure 1). Figure 2 illustrates clinical presentations by KSHV subtype. Limitations in sequencing technology and study design permit no inferences on possible associations between KSHV subtype and KS onset or severity. We observed a larger proportion of subtypes B and F, typical of African populations, in participants with KS, than those with no KAD (8/27 subtypes detected vs 3/37). However, A and C were the most commonly identified subtypes in KS (19/27 subtypes in those with KS vs 32/37 subtypes in those without KS), including in advanced cases (i.e. T1 stage, 10/13).Figure 2:KSHV Subtypes and Clinical Presentation Conclusion In conclusion, we observed extreme diversity in KSHV genomes sequenced in a single institution in Dallas, TX. Further studies are needed to better understand the relationship between viral genetics and KSHV epidemiology and disease risk in the southern US. Disclosures Ank E. Nijhawan, MD, MPH, MSCS, Gilead Sciences: Grant/Research Support