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Occupational risks of infection are similar in HCV and HIV. In 1998, 800,000 healthcare professionals reported needle-stick injuries; these resulted in 40 cases of HIV and 2000 cases of HCV infection.1

Risk factors are not limited to exposure to blood and blood products, or even mucosal routes of transmission. Studies by the Centers for Disease Control estimated the influence of poverty as well as direct exposure in order to establish risk factors for HCV infection3:

Intravenous drug use 38%
Sex with multiple partners or a partner known to have HCV 15%
Low socioeconomic status 38%
Other factors 9%

Reducing the risk of HCV in the general population and among those with HIV infection will require extensive community outreach services and patient education programs (see the two accompanying sidebars “Summary Against a Tide of Ignorance” and “Confidential HCV+ Screener”).

HIV/HCV coinfection
Coinfection with HIV and HCV is reaching epidemic proportions in this country and poses a serious treatment challenge. To meet this challenge, an aggressive nationwide program of HCV screening will be required.

Widespread screening for HCV is critical because it would permit earlier diagnosis and treatment of HCV. Early treatment is essential for two reasons: First, HCV infection can accelerate HIV progression; second, HCV causes increased liver damage in coinfected people.

Actually HIV and HCV mutually accelerate each other’s effects. There is some controversy over the role of HCV in hastening HIV progression. Studies before the era of HAART did not find enhanced HIV progression in the presence of HCV infection. However, many newer studies indicate that HCV, especially genotype 1 HCV, does cause more rapid progression to AIDS.

HIV also accelerates HCV, leading the U.S. Public Health Service in 1999 to call HCV the newest opportunistic infection of HIV. HCV viral loads increase after HIV infection. HIV infection also leads to more rapid liver damage in people with HCV. For example, having HCV alone means being about 16 times more likely to die from end-stage liver disease, while being coinfected means the odds of fatal liver disease increase 100-fold.1

Without treatment of HCV, liver damage is clearly associated with death in many coinfected people. In attempting to explain why, Dove and colleagues from the University of California at San Francisco studied the pathogenesis of this complex virus. They determined that HCV species sustain more mutations (diversity or variation) when the person’s CD4 count is less than 200 cells per microliter. The greater number of mutations may be associated with a more virulent species of virus.

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