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. 2013 Nov 25;6(12):1507-42.
doi: 10.3390/ph6121507.

Aptamer-based therapeutics: new approaches to combat human viral diseases

Ka-To Shum  1 , Jiehua Zhou, John J Rossi
Affiliations

Aptamer-based therapeutics: new approaches to combat human viral diseases

Ka-To Shum et al. Pharmaceuticals (Basel). .

Abstract

Viruses replicate inside the cells of an organism and continuously evolve to contend with an ever-changing environment. Many life-threatening diseases, such as AIDS, SARS, hepatitis and some cancers, are caused by viruses. Because viruses have small genome sizes and high mutability, there is currently a lack of and an urgent need for effective treatment for many viral pathogens. One approach that has recently received much attention is aptamer-based therapeutics. Aptamer technology has high target specificity and versatility, i.e., any viral proteins could potentially be targeted. Consequently, new aptamer-based therapeutics have the potential to lead a revolution in the development of anti-infective drugs. Additionally, aptamers can potentially bind any targets and any pathogen that is theoretically amenable to rapid targeting, making aptamers invaluable tools for treating a wide range of diseases. This review will provide a broad, comprehensive overview of viral therapies that use aptamers. The aptamer selection process will be described, followed by an explanation of the potential for treating virus infection by aptamers. Recent progress and prospective use of aptamers against a large variety of human viruses, such as HIV-1, HCV, HBV, SCoV, Rabies virus, HPV, HSV and influenza virus, with particular focus on clinical development of aptamers will also be described. Finally, we will discuss the challenges of advancing antiviral aptamer therapeutics and prospects for future success.

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Figures

Figure 1
Figure 1
(A) HIV-1 genome and (B) HIV-1 virion and potential antiviral targets.
Figure 2
Figure 2
(A) Aptamer-siRNA conjugates. The 2'-F-modified gp120 aptamer was covalently appended to the sense strand of a tat/rev siRNA portion, which in turn was hybridized to the antisense strand. A 4-nt linker (CUCU) was inserted between the aptamer and siRNA portions to minimize steric interference of the gp120 aptamer with Dicer processing [143]. (B) Aptamer-stick-siRNA chimeras. The 2'-F-modified gp120 aptamer and the siRNAs are shown. The antisense of the siRNA is linked to the aptamer portion by the stick sequence, which consists of 16 nt appended to the 3' end of the gp120 aptamer, allowing complementary base-pairing of one of the two siRNA strands with the aptamers [83].
Figure 3
Figure 3
Representation of the secondary structure of HCV IRES. Structural domains are shown as I–IV. The HH363 cleavage site is indicated by an arrow.
See this image and copyright information in PMC

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