Virus infectivity

Infection of animals Infection of man Method of virus infection... 

FIGURE 1.25 The virus life cycle. Viruses are mobile bits of genetic iuformatiou encapsulated in a protein coat. The genetic material can be either DNA or RNA. Once this genetic material gains entry to its host cell, it takes over the host machinery for macromolecular synthesis and subverts it to the synthesis of viral-specific nucleic acids and proteins. These virus components are then assembled into mature virus particles that are released from the cell. Often, this parasitic cycle of virus infection leads to cell death and disease. 

Therapeutic potential of cidofouvir, (S)-l-[3-hydroxy-2-(phosphonomethoxy) propyl]cytosine (HPMPC) for the treatment of DNA virus infections 98CCC480. 

Rhesus monkey kidney infected with Semliki Forest arborvirus gave interferon of tltre 1.5 log interferon units/2 ml. (The interferon unit, determined in a volume of 2 ml, is the dilution of interferon which produced a half-maximal score for degree of cytopathic effect In virus-infected tissue culture tubes at the time when the control without interferon first showed the maximal score.)... 

Lesion formation represents a host response to virus infection. Factors preventing the formation of starch lesions incited by the virus do not necessarily mean that virus replication is inhibited at the same time. Therefore, the total virus titer in cotyledon samples treated with different concentrations of tannic acid was determined (Figure... 

In both cases, a seeming virus stimulator (twinberry extract) and a virus inhibitor (tannic acid) operated in a more or less similar way in the cucumber-TMV system. They both affect the host defense mechanism against virus infection. The active component in twin-berry extract exhibits a mild and temporary interference, thus permitting virus to make further rounds of gain (ringlike patterns) while tannic acid produces a strong and permanent interference. 

For the pathogenesis of multiple sklerosis, autoimmune T-lymphocy tes play a predominant role, which are directed against components of the neural myelin sheath. T-lymphocy tes by secreting cytokines such as interferon y maintain the chronic inflammation which destructs the myelin sheath. Also cytotoxic T-lymphocytes may participate directly. The cause of multiple sklerosis is unknown. Significantly increased antibody titers against several vitusses, mostly the measles virus, point to a (latent) virus infection initiating the disease. 

With respect to targeting viral gene products expressed in virus-infected cells, it should be considered that infectious mammalian viruses may express inhibitors of RNAi similar to plant viruses. 

Acyclovir (Zovirax) and penciclovir (Denavir) are the only topical antiviral dragp currently available These dragp inhibit viral replication. Acyclovir is used in the treatment of initial episodes of genital herpes, as well as heqies simplex virus infections in immunocompromised patients (patients with an immune system incapable of fighting infection). Penciclovir is used for the treatment of recurrent herpes labialis (cold sores) in adults. 

La, T.N.B. Latchman, D.S. (1988). A cellular protein related to heat shock protein 90 accumulates during herpes simplex virus infection and is overexpressed in transformed cells. Exp. Cell Res. 178, 169-179. 

Phillips, B. Morimoto, R.I. (1991). Transcriptional regulation of human hsp70 genes Relationship between cell growth, dilTeientiation, virus infection, and the stress response. In Results ... 

When considering anti-infective therapy, one first thinks of a curative treatment, aiming at the rapid elimination of the pathogen from the human organism. This concept holds true for the treatment of most bacterial infections with antibiotics however, in the case of antiviral therapy, a curative treatment is the exception rather than the rule. Many human virus infections are characterized by an acute, self-limiting... 

Gripon P, Cannie I, Urban S (2005). EfScient inhibition of hepatitis B virus infection by acylated peptides derived from the large viral surface protein. J Virol 79 1613-1622 Harris RS, Liddament MT (2004) Retroviral restriction by APOBEC proteins. Nat Rev Immunol 4 868-877... 

Petersen J, Dandri M, Mier W, Lfltgehetmann M, Volz T, von Weizsacker F, Haberkom U, Fischer L, Pollok JM, Erbes B, Seitz S, Urban S (2008) Prevention of hepatitis B virus infection in vivo by entry inhibitors derived from the large envelope protein, Nat Biotechnol 26 335-341 PorniUos O, Garrus JE, Sundquist WI (2002) Mechanisms of enveloped RNA virus budding. Trends CeU Biol 12 569-579... 

Hurwitz SJ, Schinazi RF (2002) Development of a pharmacodynamic model for HIV treatment with nucleoside reverse transcriptase and protease inhibitors. Antiviral Res 56 115-127 Hurwitz SJ, Tennant BC, Korba BE, Gerin JL, Schinazi RF (1998) Pharmacodynamics of (—)-beta-2, 3 -dideoxy-3 -thiacytidine in chronically virus-infected woodchucks compared to its pharmacodynamics in humans, Antimicrob Agents Chemother 42 2804-2809 Hurwitz SJ, Otto MJ, Schinazi RF (2005) Comparative pharmacokinetics of Racivir, (+/-)-beta-2, 3 -dideoxy-5-fluoro-3 -thiacytidine in rats, rabbits, dogs, monkeys and HIV-infected humans, Antivir Chem Chemother 16 117-127... 

Shepard CW, Finelli L, Alter MJ (2005) Global epidemiology of hepatitis C virus infection. Lancet Infect Dis 5 558-567... 

Quenelle DC, Collins DJ, Wan WB, Beadle JR, Hostetler KY, Kern ER (2004) Oral treatment of cowpox and vaccinia virus infections in mice with ether Upid esters of ddofovir. Antimicrob Agents Chemother 48 404-412... 

Compound 34 (BCZ-1812, RWJ-270201, peramivir) showed selective inhibition of influenza virus sialidases over bacterial and mammalian sialidases (Babu et al. 2000 Bantia et al. 2001 Sidwell and Smee 2002). Successful inhibition of influenza virus infectivity in vitro (Smee et al. 2001) and upon oral administration in vivo [mice (Bantia et al. 2001) and ferrets, reviewed in Sidwell and Smee 2002] led to human clinical trials of orally administered peramivir (Barroso et al. 2005). While orally administrated peramivir successfully completed animal studies and Phase I and Phase II clinical trials, in which the compound was showing neither major side effects nor toxicity (Sidwell and Smee 2002), preliminary results of the Phase III trials (June 2002) demonstrated no statistically significant difference in the primary efficacy endpoint, possibly due to low bioavailability (Barroso et al. 2005). 

In the clinical setting, zanamivir 12 and oseltamivir 19 are effective in both the prevention and treatment of influenza A and B infection. Benefit in treatment is restricted to patients treated within 48 h of symptom onset (Fleming 2003). Importantly, the effects of drug treatment are a rednction in the severity of illness, and in the incidence of secondary complications. The term of illness is generally rednced between 1 and 2.5 days. The evalnation of zanamivir (Calfee and Hayden 1998 Oxford 2000 Fleming 2003), oseltamivir (Doncette and Aoki 2001 Oxford 2005) and peramivir (Sidwell and Smee 2002) for the treatment, and prophylaxis, of inflnenza virus infection has been reviewed. The reader is directed to these reviews for further details of drug pharmacodynamics and clinical trial data. 

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