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11th International AIDS ConferenceVancouver, British Columbia — July 7-12, 1996 |
Int Conf AIDS 1996 Jul 7-12; 11:57 (abstract no. Mo.A.1007)
Murakami T, Hamamoto Y, Asagami C, Yamamoto M, Handa S, Taki T, Mizuochi T, Yoshida K, Yamamoto N; Tokyo Medical and Dental University, Tokyo, Japan. Fax: 81-35803-0124. E-mail: murakami.mmb@med.tmd.ac.jp.
OBJECTIVE: To investigate the roles of sialic acid residues both on HIV-1 and target cells on the virus infectivity.
METHODS: HIV-1HTLV-IIIB and MT-4 or YAA cells (a non-tumorous monocyte/macrophage lineage cell line) were treated with a bacterial neuraminidase in the presence or absence of a specific inhibitor of the enzyme, 2,3-dehydro-2-deoxy-N-acetyl-neuraminic acid (DD-NA-NA). The effects of the enzyme treatment on the virus infectivity and the virus binding to both cell lines were examined.
RESULTS: Treatment of the virus with more than 0.4 U/ml of neuraminidase enhanced its infectivity in MT-4 cells by 30 to 60%. Furthermore, the infectivity of neuraminidase-treated virus in YAA cells, which are rather resistant to T cell line-tropic HIV-1 infection, was 4 to 10 times greater than that of untreated virus. On the other hand, the virus infectivity was decreased when both cell lines were treated with the enzyme. DD-NA-NA inhibited these effects in a dose dependent manner. Change of the virus infectivity was well correlated with that of the virus binding to the target cells.
CONCLUSIONS: Our results indicate that sialic acids on HIV-1 have negative effect for the virus infectivity, whereas those on cell surface are necessary for the virus infection in at least certain cell lines. The enhanced infectivity by neuraminidase treatment is due to increased binding capacity of the treated virus to the target cells. However, the precise mechanism of effects of neuraminidase treatment requires further study.
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MoA1007
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