Viruses evolution

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The broadest spectrum of antiviral diugs is available against HIV. However, monotherapy with any of these diugs leads to rapid treatment failure due to selection and further evolution of resistant viruses. Since acquisition of resistance mutations requires vims replication,... 

Short replication cycles that may be completed within a few hours, a large amount of viral progeny from one infected host-cell, as well as the general inaccuracy of viral nucleic acid polymerases result in an evolution occurring in fast motion, allowing rapid adaptation of viruses to selective pressures (see chapter by Boucher and Nijhius, this volume). Generalizing, it can be stated that any effective antiviral therapy will lead to the occurrence of resistance mutations. A well studied example... 

Abstract This review provides an overview of the development of viral protease inhibitors as antiviral drugs. We concentrate on HlV-1 protease inhibitors, as these have made the most significant advances in the recent past. Thus, we discuss the biochemistry of HlV-1 protease, inhibitor development, clinical use of inhibitors, and evolution of resistance. Since many different viruses encode essential proteases, it is possible to envision the development of a potent protease inhibitor for other viruses if the processing site sequence and the catalytic mechanism are known. At this time, interest in developing inhibitors is Umited to viruses that cause chronic disease, viruses that have the potential to cause large-scale epidemics, or viruses that are sufQciently ubiquitous that treating an acute infection would be... 

Antiviral Resistance and Impact on Viral Replication Capacity Evolution of Viruses Under Antiviral Pressure Occurs in Three Phases... 

In this chapter we describe the current insights into the evolution of viruses under pressure of antiviral therapy and the potential impact on viral fimess. As most recent work in this field has been done in the field of human immunodeficiency virus (HIV), we use the evolution of this virus as the basis for the chapter. Subsequently, we describe resistance evolution for Hepatitis B virus (HBV), where large progress has been made in recent years. Furthermore, we describe the resistance development for Hepatitis C virus (HCV), for which a very active drug development program is undertaken by several pharmaceutical companies. Finally, we discuss resistance evolution for Influenza. 

Initially, it was assumed that the HlV-1 population is infinite, evolution is deterministic, and antiretroviral resistance development is definite (Coffin 1995). However, our research amongst others has demonstrated that the effective population size, defined as the average number of HIV variants that produces infectious progeny is relatively small (Leigh Brown 1997 Leigh Brown and Richman 1997 Nijhnis et al. 1998). This can be explained because the majority of virus particles that are produced harbor deleterious mutations resulting in noninfectious virus. Also limited target cell availability and inactivation of potentially infectious viruses by the host... 

Fig. 1 Three phases in viral evolution during suboptimal therapy. The black hne represents wild type virus, whereas the red line represents mutant virus (Res stands for the level of resistance and RC for replication capacity).

The evolution of antiviral resistance for viruses discussed in this chapter (HIV, HBV, HCV, and Influenza virus) shares some common features. Replication in vivo results in the generation of viral variation and selection of preexisting viruses from the population occurs under particular conditions. This will only happen when the escaping viruses have a sufficient level of both resistance and RC. In most cases, the resistance level subsequently increases further by the gradual acquisition of further mutations. Additional compensatory mutations then accumulate that help to restore full RC in the third stage. 

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Nelson CJ, Carrigan KA, Lysle DT (2000) Naltrexone administration attenuates surgery-induced immune alterations in rats. J Surg Res 94(2) 172-177 Noel RJ Jr, Kumar A (2006) Virus replication and disease progression inversely correlate with SIV tat evolution in morphine-dependent and SIV/SHIV-infected Indian rhesus macaques. Virology 346(1) 127-138... 

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