Abstract
The major immediate-early (IE) gene of human cytomegalovirus (CMV) is believed to have a decisive role in acute infection and its activity is an important indicator of viral reactivation from latency. Although a variety of gene products are expressed from this region, the 72-kDa IE1 and the 86-kDa IE2 nuclear phosphoproteins are the most abundant and important. Both proteins have long been recognized as promiscuous transcriptional regulators. More recently, a critical role of the IE1 and IE2 proteins in counteracting non-adaptive host cell defense mechanisms has been revealed. In this review we will briefly summarize the available literature on IE1- and IE2-dependent mechanisms contributing to CMV evasion from intrinsic and innate immune responses.
Highlights
The major immediate-early (IE) gene of human cytomegalovirus (CMV) is believed to have a decisive role in acute infection and its activity is an important indicator of viral reactivation from latency
(Figure 1), the 72-kDa IE1 and the 86-kDa IE2 nuclear phosphoproteins are the most abundant and important. They share 85 amino-terminal amino acids corresponding to major IE exons 2 and 3 but have distinct carboxy-terminal parts encoded by exon 4 (IE1) or exon 5 (IE2) (Figure 1)
The first mechanism depends on binding of IFN-activatable STAT2 to the carboxy-terminal IE1 domain resulting in inhibition of ISGF3-mediated anti-viral gene induction
Summary
The predominant major IE protein species, which are the subject of this review, are highlighted in blue. It is uncertain whether the IE1 isoforms shown in gray are present in CMVinfected cells [4]. Polyadenylation and promoter usage this viral genomic region produces multiple mRNAs (reviewed in [3]). (Figure 1), the 72-kDa IE1 and the 86-kDa IE2 nuclear phosphoproteins are the most abundant and important. They share 85 amino-terminal amino acids corresponding to major IE exons 2 and 3 but have distinct carboxy-terminal parts encoded by exon 4 (IE1) or exon 5 (IE2) (Figure 1). The absence of IE1 results in severely attenuated viral replication under low MOI conditions [10,11]
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