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J Virol ; 86(12): 6434-43, 2012 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-22491462

RESUMO

Herpes simplex virus 2 (HSV-2) is the primary cause of genital herpes, which is one of the most common sexually transmitted viral infections worldwide and a major cofactor for human immunodeficiency virus infection. The lack of an effective vaccine or treatment and the emergence of drug-resistant strains highlight the need for developing new antivirals for HSV-2. Here, we demonstrate that a low-molecular-weight peptide isolated against 3-O-sulfated heparan sulfate (3-OS HS) can efficiently block HSV-2 infection. Treatment with the peptide inhibited viral entry and cell-to-cell spread both in vitro and in vivo using a mouse model of genital HSV-2 infection. Quite interestingly, the peptide showed a preferential binding to HSV-2-infected cells, with more than 200% increased binding compared to uninfected cells. Our additional results show that heparan sulfate expression is upregulated by 25% upon HSV-2 infection, which is a significant new finding that could be exploited for designing new diagnostic tests and treatment strategies against HSV-2-infected cells. In addition, our results also raise the possibility that 3-OS HS modifications within HS may be upregulated even more to accommodate for a significantly higher increase in the peptide binding to the infected cells.


Assuntos
Antivirais/farmacologia , Heparitina Sulfato/antagonistas & inibidores , Herpes Genital/virologia , Herpesvirus Humano 2/efeitos dos fármacos , Peptídeos/farmacologia , Receptores Virais/antagonistas & inibidores , Animais , Linhagem Celular , Feminino , Heparitina Sulfato/metabolismo , Herpes Genital/tratamento farmacológico , Herpes Genital/metabolismo , Herpesvirus Humano 2/fisiologia , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Receptores Virais/metabolismo , Internalização do Vírus/efeitos dos fármacos
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