Introduction and Background

A major stumbling block to culture HCV in vitro has been the difficulty of its integration into host genome (Our initial patent: In Vitro Tissue Culture Assay to Screen Potential Drugs for HCV, University of California (UC) Case No. 2001-067-1 (Hepatitis C Virus), approved February 2007. Chronic HCV infection leads to HCC in 50% of the affected patients with 2-3% of the world population currently remain infected. Globally 150-170 million people are infected with HCV (Figure 1). Though the most current statistical distribution for HIV is not quoted herein, HIV prevalence globally (Figure 2) has always significantly been lower than that that of HCV.

Uncontrolled HCV infection can lead to HCC and death, so also high proviral loads of chronic HIV replication. Whereas HCV is an RNA virus, HIV despite being a lentivirus (retrovirus derivative) its provirus for integration into the human host genome is DNA, post-reverse transcription from RNA into DNA [1]. From the rapidity with which a cure for HCV has been developed it seems that the mutations in the NS3 region of HCV genome [2] could be tackled therapeutically considerably easier [3] than the yet incurable HIV infection with its extremely high mutation rate of V3 loop region of HIV (-1) [4].

Discussion

Interferon-α (IFN-α) has long been known to carry anti-viral efficacy including against HCV but with some confined virus species specific effectiveness particularly with reference to inaction against HIV. IFN-α is known for its side effects and hence initial anti-HCV treatments using IFN-α were not successful. In recent times following development of HCV specific drugs that have been developed, the need for using IFN-α in a combination therapy is significantly, if not dramatically reduced. Such single use drugs are developed in 2014 and include ledipasvir and sofosbuvir, the latter comes in an easy once-a-day pill. It takes as few as 12 weeks to work, and it cures up to 90% of HCV infected patients.

Discussion

It is heartening to note that cure for HCV is well on its way through advancement into further generations, but for HIV it is still elusive though to-date the longevity of the infected patients is greatly increased and with fewer side effects.

1. Ogata N, Alter HJ, Miller RH, Purcell RH (1991) Nucleotide sequence and mutation rate of the H strain of hepatitis C virus. Proc Natl Acad Sci USA 88(8); 3392-3393.
2. Chen KX, Njoroge FG (2009) A review of HCV protease inhibitors. Current Opinion in Investigational Drugs (London, England: 2000). 10(8): 821-837.
3. Deeks SG, Smith M, Holodniy M, Kahn JO (1997) A review for clinicians JAMA 277(2): 145-153.
4. Zhang M, Evans S, Yuan J, Ratner L, Koka PS (2010) HIV-1 determinants of thrombocytopenia at the stage of CD34+ progenitor cell differentiation in vivo lie in the viral envelope gp120 V3 loop region. Virology 401(2): 131-136.

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  Figure 1: Global prevalence of chronic hepatitis C virus infection (reprinted from Holmberg S [Holmberg S. CDC Health Information for International Travel 2012 (yellow book).Oxford, UK: Oxford University Press; 2012. Hepatitis C; p. 186-187.Google Scholar]).

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  Figure 2: As of 2009, it is estimated that there are 33.3 million people worldwide infected with HIV. ( “Worldwide AIDS & HIV Statistics”. AVERT. 31 December 2009. Archived from the original on 2011-04-06.Retrieved 26 January 2011). AIDS_and_HIV_prevalence.svg: Escondites derivative work: Furfur HIV PREVALENCE MAP: A poster sized map and companion chart provides a global view of HIV prevalence in 2009 (UNAIDS) - This file was derived from AIDS and HIV prevalence.svg:
  HIV/AIDS prevelance world map in 2009 according to UNAIDS data.
  (15-49) per country at the end of 2009.
  0.1 %
  0.1-0.5 %
  0.5-1 %
  1-5 %
  5-15 %
  15-50 %