Although HIV-1 does not induce a rapid and dramatic global shutdown of host cell translation following infection, in contrast to other viruses such as poliovirus, cap-dependent translation initiation is decreased due to cellular stress following infection by this virus (25, 45) and this decrease can be related to PKR activation (46) . Our results suggest that a change in cap-dependent translation initiation could affect HIV-1 frameshift efficiency in infected cells. As mentioned in the 'Introduction' section, the virus replication appears to be exquisitely sensitive to changes in frameshift efficiency. Given the detrimental effect of such changes, the virus likely uses various strategies to counteract this effect. One strategy is inhibition of PKR (reviewed in 25, 47) to stimulate translation initiation. HIV-1 uses two major ways to inhibit PKR: its Tat protein inhibits PKR and its TAR RNA structure blocks PKR dimerization when present in large quantities. TAR is located at the 5 0 and 3 0 end of all HIV-1 mRNAs and is also present under a free cytoplasmic form of 58-66 nt (17, 18) . All these forms of TAR can participate in the inhibition of PKR.