In vitro inhibition of dengue virus entry by p-sulfoxy-cinnamic acid and structurally related combinatorial chemistries

Rees, Craig R; Costin, Joshua M.; Fink, Ryan C.; McMichael, Matthew; Fontaine, Krystal A.; Isern, Sharon; Michael, Scott F.

doi:10.1016/j.antiviral.2008.05.007

Cited by 53 publications

(38 citation statements)

References 36 publications

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“…Inhibitory activities by both extract and alkaloidal fraction of Uncaria tomentosa on infection rates and cytokine levels in treated monocytes-DENV infected have been reported (Reis et al 2008). It seems that the zosteric acid derived from Zostera marina interferes with binding to the receptor required for DENV entry into the host cell (Rees et al 2008). Anti-dengue activity of Hippophae rhamnoides leaf extract was demonstrated in DENV-2 infected blood-derived human macrophages (Jain et al 2008).…”

Section: Resultsmentioning

confidence: 99%

Virucidal activity of Colombian Lippia essential oils on dengue virus replication in vitro

Ocazionez

Meneses

Torres

et al. 2010

Mem. Inst. Oswaldo Cruz

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The inhibitory effect of Lippia alba and Lippia citriodora essential oils on dengue virus serotypes replication in vitro was investigated. The cytotoxicity (CC 50 ) was evaluated by the MTT assay and the mode of viral inhibitory effect was investigated with a plaque reduction assay. The virus was treated with the essential oil for 2 h at 37 o C before cell adsorption and experiments were conducted to evaluate inhibition of untreated-virus replication in the presence of oil. Antiviral activity was defined as the concentration of essential oil that caused 50% reduction of the virus plaque number (IC 50 ). L. alba oil resulted in less cytotoxicity than L. citriodora oil (CC 50 : 139.5 vs. 57.6 µg/mL). Virus plaque reduction for all four dengue serotypes was observed by treatment of the virus before adsorption on cell. The IC 50 values for L. alba oil were between 0. 4-32.6 µg/mL and between 1.9-33.7 µg/mL for L. citriodora oil. No viral inhibitory effect was observed by addition of the essential oil after virus adsorption. The inhibitory effect of the essential oil seems to cause direct virus inactivation before adsorption on host cell.Key words: essential oil -antiviral -virucidal activity -dengue virus -Lippia sp.Dengue is an acute illness characterised by the hemorrhagic fever caused by dengue virus (DENV) that is transmitted to humans by Aedes mosquitoes. DENV infection results in a spectrum of disease ranging from a mild febrile illness or dengue fever to a severe disease or dengue hemorrhagic fever/dengue shock syndrome. Among the human arboviral diseases, dengue is responsible for causing most illness and death. It has been estimated that 50-100 million dengue infections occur each year in tropical urban areas around the world with 20,000-25,000 deaths (Gubler 2006).DENV is a member of the Flaviviridae family and it exists as four related serotypes (DENV-1 2, 3 and 4). The virus possesses an icosahedral nucleocapsid core surrounded by a host-derived lipid membrane (envelope), in which the envelope (E) protein and membrane (M) protein are embedded. The Flavivirus enters into the host cell by receptor-mediated endocytosis into coated vesicles, a process in which the E protein plays the major role. The E protein mediates interactions within the virus and the components of the host cell membrane involved in virus adsorption and the E protein interacts with the membrane cell during fusion (Lindenbach & Rice 2007). Compounds that interact with sites on the E protein that binds to structures on the cellular membrane affect the adsorption and fusion process. That interferes There is no antiviral drug for treatment for any of the Flavivirus and an effective vaccine for human use is not yet available to prevent dengue. Consequently, the development of antiviral drugs licensed for treatment of patients remains an urgent need to prevent dengue fatalities. Compounds obtained from traditional medicinal plants and herbs species have been reported to have antiviral activity and a wide variety of active phytochemicals hav...

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Section: Resultsmentioning

confidence: 99%

Virucidal activity of Colombian Lippia essential oils on dengue virus replication in vitro

Ocazionez

Meneses

Torres

et al. 2010

Mem. Inst. Oswaldo Cruz

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“…Blockade of virus uncoating [135] E hydrophobic pocket target peptides Unknown [136] E hydrophobic pocket target small molecules Unknown [137,138] Zosteric acid derivatives Unknown [139] CBA: Carbohydrate-binding agent; E: Viral glycoprotein; GNA: Galanthus nivalis agglutinin; HHA: Hippeastrum hybrid agglutinin; mAb: Monoclonal antibody; UDA: Urtica dioica agglutinin.…”

Section: Carrageenans Inhibition Of Virus Adsorption and Penetrationmentioning

confidence: 99%

Dengue Virus Entry and Trafficking: Perspectives as Antiviral Target for Prevention and Therapy

2015

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Dengue virus (DENV) is the etiological agent of the most important human viral infection transmitted by mosquitoes in the world. In spite of the serious health threat that dengue represents, at present there are no vaccine or antiviral agents available and treatment of patients consists of supportive therapy. This review will focus on the process of DENV entry into the host cell as a potential target for antiviral therapy. The recent advances in the knowledge of viral and cellular molecules and mechanisms involved in binding, internalization and trafficking of DENV into the host cell until virion uncoating are discussed, together with an overview of the strategies and compounds evaluated for development of antiviral agents targeted to DENV entry. KeywordsDengue is currently the most widespread arbovirosis in the world, with a particularly high prevalence in diverse tropical and subtropical regions of America and Asia [1]. The WHO estimates an occurrence of 50-100 million annual infections, but more recent modelling evaluations increased the number of new possible infections to 390 million per year [2]. There are four serotypes of dengue viruses (DENV), designated DENV-1 to DENV-4, that cocirculate and are transmitted to humans by the bites of the mosquitoes Aedes aegypti and Aedes albopictus. Precisely, the failure in the programs for control of the mosquito vector is one of the reasons for the explosive re-emergence and global spread of dengue in the last few decades in >100 countries, resulting in a serious public health challenge.All serotypes can produce either an inapparent infection or a wide spectrum of clinical outcomes ranging from a mild febrile illness known as dengue fever (DF) to the more severe and life-threatening forms of dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) [3]. The initial infection with one DENV serotype leads to lifelong protection against homologous reinfection, but only brief and partial protection against infection with other serotypes. In fact, the secondary infection with a heterologous serotype is considered a risk factor for developing DHF and DSS. These severe clinical manifestations have been associated to the phenomenon known as antibody-dependent enhancement (ADE) [3]. In this process, the antibodies elicited by the primary infection bind to the heterotypic virus without neutralization of viral infectivity, and these immune complexes are opsonized into Fc-receptor positive cells leading to an increase in DENV replication and pathogenesis [4,5].DENV is a member of the genus Flavivirus in the family Flaviviridae. The virion is a small spherical particle, 40-50 nm in diameter, containing a single-stranded positive sense RNA included in an inner nucleocapsid and surrounded by a lipid envelope. The virus genome codes for a single polyprotein that is cleaved into three structural proteins (the capsid protein C,

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“…For dengue, a p-sulfoxy-cinnamic acid derivative (CF-238) has been described as a virus entry inhibitor, showing albeit rather weak activity against all four dengue virus types. 172 The binding (adsorption) of dengue virus to its target cells can be effectively blocked by sulfated polysaccharides (such as heparin and heparan sulfate) and polysulfonates (such as suramin) 173 [for a further description of suramin and polysulfonates as compared to polysulfates, see De Clercq 2 ]. Heparan sulfate, 174 sulfated galactomannans, 175 and i-, l-, and k-carrageenans 176 have been shown to inhibit dengue virus binding to the host cells, albeit highly depending on the virus type, Dengue type 2 being the most sensitive.…”

Section: Ten Stories On Antiviral Drug Discovery K 681mentioning

confidence: 99%

Yet another ten stories on antiviral drug discovery (part D): Paradigms, paradoxes, and paraductions

Clercq

2009

Medicinal Research Reviews

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This review article presents the fourth part (part D) in the series of stories on antiviral drug discovery. The stories told in part D focus on: (i) the cyclotriazadisulfonamide compounds; (ii) the {5-[(4-bromophenylmethyl]-2-phenyl-5H-imidazo[4,5-c]pyridine} compounds; (iii) (1H,3H-thiazolo[3,4-a]benzimidazole) derivatives; (iv) T-705 (6-fluoro-3-hydroxy-2-pyrazinecarboxamide) and (v) its structurally closely related analogue pyrazine 2-carboxamide (pyrazinamide); (vi) new strategies for the treatment of hemorrhagic fever virus infections, including, as the most imminent, (vii) dengue fever, (viii) the veterinary use of acyclic nucleoside phosphonates; (ix) the potential (off-label) use of cidofovir in the treatment of papillomatosis, particularly RRP (recurrent respiratory papillomatosis); and (x) finally, the prophylactic use of tenofovir to prevent HIV infections.

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In vitro inhibition of dengue virus entry by p-sulfoxy-cinnamic acid and structurally related combinatorial chemistries

Cited by 53 publications

References 36 publications

Virucidal activity of Colombian Lippia essential oils on dengue virus replication in vitro

Virucidal activity of Colombian Lippia essential oils on dengue virus replication in vitro

Dengue Virus Entry and Trafficking: Perspectives as Antiviral Target for Prevention and Therapy

Yet another ten stories on antiviral drug discovery (part D): Paradigms, paradoxes, and paraductions

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