The discovery that inoculation of DNA leads to strong and long lasting immune responses generated enthusiasm to assess the efficacy of various genetically engineered vaccines against mucosally acquired infections. Various techniques have been used to generate the most suitable DNA vaccines, ranging from immunization with naked DNA to utilizing genetically engineered recombinant viruses and bacteria to deliver the DNA. Different DNA vaccine modalities and mucosal immune responses to them have been discussed. It has been shown that even though intramuscular and intradermal immunization with these vaccines generates strong systemic responses, mucosal responses are not induced. It has been proposed that the site of immunization determines mucosal immune responses and that primed lymphocytes preferentially accumulate at sites where they have been induced thus generating the strongest cellular and antibody responses at the site of vaccination. The impact of the site of induction on mucosal immune responses to vaccines is discussed. It is possible to enhance desired vaccine effects in the mucosa and to modify the undesirable side effects. Cytokines such as IL-2, IL-12, IL-15 and IL-18 have been used to enhance CTL activity while IL-5, IL-6 and the chemokine MIP-1␣ have shown the capacity to increase IgA responses to vaccines. Genes and Immunity (2000) 1, 308-315.
To determine HIV-1 subtypes and antiretroviral drug resistance mutations for 16 infected, pregnant women in Jos, Nigeria, part of pol (1040 bp) was amplified from patient PBMC DNA, sequenced and analyzed. Eight of the samples were subtype G, three were CRF02_AG and 2 were unique recombinant forms (URF) between G and CRF02_AG. The remaining consisted of 3 different strains: one was subtype C, and the other 2 were unrelated URF. Nearly full-length genome sequences were completed for 6 of the strains: 4 subtype G and 2 CRF02_AG. In the 14 drug-naïve subjects, no primary resistance-associated mutations were found, but secondary mutations were identified in 7 different codons of the gene coding for protease: PR K20I, M36I, L63A/P/V, V82I, L10M/I and I93L. In addition, the K238R mutation was identified in the reverse transcriptase gene of 3 viruses. The PR K20I and M36I mutations occurred in all of the strains, and the L10M and V82I mutations occurred only in subtype G. The mutation, I93L, was carried by subtype C viruses. Two of the women that had prior niverapine treatment, had primary resistance-associated mutations, RT M184V and K103N, archived in their proviral DNA several months after treatment cessation. The study reports a predominance of clade G and CRF02_AG, and provides many more examples of nearly full-length genome sequences for subtype G viruses from Nigeria. The ubiquitous presence of PI secondary resistance-associated mutations, as well as primary resistanceassociated mutations in 2 previously treated women, underscores the need to ensure adherence compliance to treatment.
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