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PubMed2000

Multidrug resistance genotypes (insertions in the beta3-beta4 finger subdomain and MDR mutations) of HIV-1 reverse transcriptase from extensively treated patients: incidence and association with other resistance mutations.

Multiple nucleoside resistance involves specific mutational patterns of the HIV-1 pol gene that are independent of the classic mutations conferring resistance to individual dideoxynucleosides. These include a cluster of five mutations in the reverse-transcriptase (RT) coding region (A62V, V75I, F77L, F116Y, and Q151M) generally referred to as multidrug resistance (MDR) mutations, and insertions of one or several amino acid residues between codons 67 and 70 of RT, a flexible region joining two antiparrallel beta sheets (beta3-beta4 insertions). The objectives of this study were (i) to determine the prevalence of multidrug resistance genotypes (MDR mutations and beta3-beta4 insertions) in a cohort of 632 patients who were extensively pretreated with anti-HIV drugs and not responding to their current antiretroviral therapy, and (ii) to analyze the association of multidrug resistance genotypes with other resistance mutations in the RT and protease genes. Among viruses sequenced from these patients, 15 (2.4%) of them contained an insertion and 2 (0.3%) contained a deletion in the beta3-beta4 finger subdomain of RT. In 9 cases, the insertion was associated with a D67S, G, or E mutation. In addition, we identified 13 (2.1%) viruses harboring specific MDR mutations (mainly Q151M and/or A62V, V75I, F116Y). Interestingly, the A62V mutation was found in 6 of the 15 strains with an insertion, whereas the other MDR mutations were not observed in insertion mutant strains. Especially high levels of resistance to zidovudine were observed for viruses with a beta3-beta4 insertion in the background of A62V, L210W, and T215Y. Otherwise, MDR mutations and beta3-beta4 insertions were found in association with the classic mutations conferring resistance to zidovudine, lamivudine, nonnucleoside RT inhibitors, and protease inhibitors, according to treatment history. Finally, we observed a genome with a deletion of codon 70 associated with a Q151M MDR mutation. These data suggest that the emergence of HIV-1 multidrug resistance, which may occur in various genetic contexts, poses a challenging problem in formulating treatment strategies.

Acquired Immunodeficiency Syndrome↗
PubMed1992

The gene for cadmium metallothionein from a cadmium-resistant yeast appears to be identical to CUP1 in a copper-resistant strain.

A cadmium-resistant strain of Saccharomyces cerevisiae produces a cadmium metallothionein with the same characteristics as the copper metallothionein that is encoded by CUP1 in a copper-resistant strain. The structural gene for metallothionein from the cadmium-resistant strain resembles CUP1 in terms of the fragmentation patterns generated by restriction enzymes. Furthermore, the gene may be amplified as 2.0 kb repeating units in both the cadmium-resistant and the copper-resistant strains. However, transformants with a plasmid that carried the metallothionein gene from the cadmium-resistant strain were resistant to copper but not to cadmium. It appears that the same metallothionein gene, CUP1, is amplified in both cadmium- and copper-resistant yeasts. However, the mechanism for the cadmium-specific inducibility of the gene may be restricted to the cadmium-resistant strain.

Cadmium↗