In latently infected marmoset T cells, H erpesvirus saimiri (HVS) is a T-lymphotropic gammaherpesvirus that causes acute T-cell lymphomas and leukemias inNew World primates and transforms human primary T cells in vitro (1). The most abundant transcripts in HVS latently infected marmoset T cells are seven noncoding U-rich RNAs, known as HSURs (H. saimiri U-rich RNAs) (2). The functions of these viral noncoding RNAs are not well understood. HSUR1 forms base-pairing interactions with a host microRNA (miRNA), miR-27, targeting it for rapid degradation (3). This helps to promote constitutive activation of infected T cells and viral latency (4, 5). We recently discovered that, in addition to the HSURs, HVS expresses during latency another class of noncoding RNAs: six miRNAs called miR-HSURs (6). The miR-HSURs are cotranscribed together with the HSURs to give rise to chimeric primary transcripts, which are then processed via a combination of canonical and noncanonical pathways to yield mature HSURs and miRNAs (6).In complex with Argonaute (Ago) family proteins, mature miRNAs modulate target protein levels through base pairing with their mRNAs (7). Like cellular miRNAs, viral miRNAs play key regulatory roles in gene expression in host cells (8). Previous studies suggested that viral miRNAs benefit infection and the viral life cycle through regulation of (i) viral persistence, (ii) proliferation and/or survival of the infected host cells, and (iii) host immune evasion (2). Because the functions of the miR-HSURs were unknown, we embarked on the identification of their viral and cellular targets in latently infected marmoset T cells. MATERIALS AND METHODSCell culture and transfection. Marmoset (Callithrix jacchus) T cells infected with HVS strain ⌬2A (referred to as ⌬2A cells) were generated and grown as described previously (9). They were derived from marmoset peripheral blood lymphocytes immortalized by HVS and are predominantly activated CD8 cytotoxic T cells. A 1,379-bp deletion present in the
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