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Sexual and Perinatal Spread of Hepatitis C Virus Infection

From the NIH Consensus Development Conference on Management of Hepatitis C
Title: Sexual and Perinatal Spread of Hepatitis C Virus Infection
Author: Jules L. Dienstag, M.D.

Compared with the level of viremia in patients with chronic hepatitis B, the level of viremia in patients with hepatitis C virus (HCV) infection is relatively low. This difference, by many orders of magnitude, between the concentrations of circulating virus, translates to less efficient transmission of hepatitis C from person to person. Whereas direct, percutaneous inoculation e.g., via transfusion or intravenous self-injection of addictive drugs-is very efficient in transmitting HCV infection, less direct, so-called nonpercutaneous routes of infection are inefficient in the spread of hepatitis C.

Sexual Transmission
Among patients with reported cases of acute hepatitis C in the United States, a history of sexual contact with a person at risk for HCV infection-that is, potential sexual exposure-can be elicited in approximately 10 percent of cases. (1,2) In addition, certain subpopulations with recognized frequent multipartner sexual activity, such as professional sex workers (prostitutes), promiscuous homosexual men, and persons of both sexes attending clinics for sexually transmitted diseases (STDs), have serologic markers of HCV infection that are many fold more frequent than in the general population and may reach prevalences as high as 20 percent. In some of these populations, concomitant percutaneous exposures, such as intravenous drug use, tattoos, and so on, contribute to HCV exposure, but, in some studies, the rate of HCV infection is higher in such persons with frequent, multiple sexual partners, independent of other potential risk factors. In a survey of patients presenting to a Baltimore emergency room, the frequency of anti-HCV was high, at 18 percent. (3) The frequency in homosexual men was 21 percent, not substantially different from the figure in the entire group, and the frequency was much lower, 6 percent, for those with heterosexual exposure to a partner with high-risk behavior for blood-borne infection. These findings did not point toward substantial sexual exposure to HCV, but the frequency of anti-HCV in a subset of black men between the ages of 35 and 44 was 51 percent. Although intravenous drug use is common in this decade of life in this population, sexual exposure was another hypothetical mode of exposure likely to be operative in this group. In a subsequent study of patients attending STD clinics in the same city, among 309 sexual partners of 1039 non-drug-using patients, anti-HCV was found in 7 percent of men and 4 percent of women; the risk was substantially higher primarily for female partners of men with anti-HCV, but not for male partners of women with anti-HCV, suggesting that male-to-female transmission is more efficient.4 Other risk factors in the index case that were associated with transmission to the sexual partner included HIV infection, age more than 28 years, more than 24 life-time sexual partners, other STDs and cigarette smoking. (4)

Although frequent sexual activity with multiple partners may be associated with sexual transmission of HCV infection, studies to define sexual transmission between monogamous, stable sexual partners usually fail to provide convincing evidence for efficient transmission. (5) Although several studies do show increases in serologic and virologic evidence for HCV infection in sexual partners of persons with chronic hepatitis C, several of the most definitive failed, with very rare exceptions, to detect HCV infection in sexual partners unless the partners had independent, nonsexual risk factors for acquisition of hepatitis C. (6,7) In a widely cited point-prevalence study from Japan, 18 percent of the spouses of 154 index patients with chronic hepatitis C had evidence of HCV infection, and the frequency of HCV markers increased for each decade of marriage-50 percent increase in antibody to HCV per decade and 90 percent increase in HCV RNA per decade of marriage. (8) At face value, these data suggest that sexual exposure to HCV increases continuously over time during marriage; however, the lowest frequencies of HCV infection were documented during the early years of marriage, when sexual activity is at a peak, and the highest frequencies of HCV infection were documented during very late decades of marriage, when sexual activity is substantially lower. Therefore, rather than demonstrating an increase in HCV exposure with successive decades of marriage, this point-prevalence survey appears to be detecting a cohort effect, in which older spouses were infected early in life and not necessarily via sexual contact.

A consensus is difficult to draw among the many studies reported to date of sexual transmission of hepatitis C. Given documentation of genetic homogeneity in circulating HCV between spouse pairs in some studies, given the higher frequency of HCV markers in some groups with potential sexual exposure, we cannot ignore the reality that, under certain circumstances, HCV infection can be transmitted sexually. A distinction does appear to exist, however, between promiscuous, frequent sexual activity-associated with transmission-and stable, monogamous sexual activity-rarely associated with transmission. An estimate of the likelihood of sexual transmission is on the order of 5 percent, supporting a relatively low risk of infection.

Accordingly, based on such a low risk, the U.S. Public Health Service has not recommended barrier precautions between stable, monogamous sexual partners.

Perinatal Transmission
Passive acquisition of anti-HCV from mother to baby occurs at the time of birth, but infection of the neonate is much less likely. The occasional, documented case of perinatal transmission of HCV infection notwithstanding, perinatal spread of HCV infection is uncommon. Both serologic surveys and studies in which sensitive assays are applied to detect HCV RNA in the neonate fail to document efficient transmission of sustained infection; thus, although anti-HCV and even HCV RNA can be documented after birth in babies bom to mothers with HCV infection, these infections are rarely associated with chronic infection. (9) A much-cited study from Japan demonstrated HCV transmission from mother to infant in 6 percent of babies born to mothers with anti-HCV and in 10 percent in babies born to mothers with HCV RNA. An important observation linked transmission to the level of viremia. Among babies bom to mothers whose HCV RNA levels were <106 copies per ml, no maternal-fetal transmission of HCV infection occurred; in contrast, among babies bom to mothers with circulating levels of HCV RNA, >106 copies per ml, the efficiency of transmission was as high as 36 percent. (10) Although long-temm followup monitoring of these babies was not reported, data such as these suggest that transmission can occur between mother and baby at the time of birth; however, the rarity of documented perinatal transmission of HCV infection in the United States, except perhaps in babies bom to mothers who are infected with both HCV and HIV, is consistent with the observation that high-level viremia is uncommon.

Weighing the many, often-conflicting reports conceming perinatal transmission, the Centers for Disease Control of the U.S. Public Health Service has estimated that the likelihood of perinatal transmission is low, on the order of 5-6 percent. Data collected to date show no increase in HCV infection among breast-fed babies; (11) therefore, breast feeding is not discouraged for mothers with chronic hepatitis C.

Household/lntrafamilial Transmission
Although increased frequencies of anti-HCV have been reported in household members of persons with chronic HCV infection, most studies, especially in the United States, have failed to demonstrate any serologic or virologic evidence of HCV transmission to nonsexual partners within households. (5) Current data, therefore, do not support household exposure as a risk for HCV infection.

Although sexual and perinatal routes may play a small role in the transmission of HCV infection, neither is considered an efficient mode of exposure to HCV; the likelihood of such exposures is approximately 5 percent. Household/familial contact is not considered a risk factor for the transmission of hepatitis C. Common-sense precautions between sexual partners include avoidance of the interchange of body fluids and shared percutaneous exposures, but barrier precautions are not recommended routinely for monogamous, stable partners. For persons with multiple sexual partners, "safe-sex" precautions, including the use of latex condoms, should be recommended. Because of the low risk of perinatal transmission, data are insufficient to support the interdiction of pregnancy in women with chronic hepatitis C, screening of pregnant women for HCV infection is not recommended, and breast feeding is permitted. There is no known prophylaxis with globulin against sexual or perinatal HCV infection.

1. Alter MJ, Coleman PJ, Alexander WJ, et al. Importance of heterosexual activity in the transmission of hepatitis B and non-A, non-B hepatitis. JAMA 1989;262:1201-5.
2. Alter MJ, Hadler SC, Judson FN, et al. Risk factors for acute non-A, non-B hepatitis in the United States and association with hepatitis C virus infection. JAMA 1990;264:2231-5.
3. Kelen GD, Green GB, Purcell RH, et al. Hepatitis B and hepatitis C in emergency department patients. N Engl J Med 1992;326:1399-1404.
4. Thomas DL, Zenilman JM, Alter HJ, et al. Sexual transmission of hepatitis C virus among patients attending sexually transmitted disease clinics in Baltimore-An analysis of 309 sex partnerships. J Infect Dis 1994;171:768-75.
5. Everhart JE, Di Bisceglie AM, Murray LM, et al. Risk for non-A, non-B (type C) hepatitis through sexual or household contact with chronic carriers. Ann Intern Med 1990;112:544-5.
6. Weinstock HS, Bolan G, Reingold AL, Polish LB. Hepatitis C virus infection among patients attending a clinic for sexually transmitted diseases. JAMA 1993;269:392-4.
7. Osmond DH, Padian NS, Sheppard HW, Glass S, Shiboski SC, Reingold A. Risk factors for hepatitis C virus seropositivity in heterosexual couples. JAMA 1993;269:361-5.
8. Akahane Y, Kojima M, Sugai Y, et al. Hepatitis C virus infection in spouses of patients with type C chronic liver disease. Ann Intem Med 1994;120:748-52.
9. Reinus JF, Leikin EL, Later HJ, et al. Failure to detect vertical transmission of hepatitis C virus. Ann Intern Med 1992;1 17:881-6.
10. Ohto H, Terazawa S, Sasaki N, et al. Transmission of hepatitis C virus from mothers to infants. N Engl J Med 1994;330:744 50.
11. Zanetti AR, Tanzi E, Paccagnini S, et al. Mother-to-infant transmission of hepatitis C virus. Lancet 1995;345:289-91.

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