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.
Conclusion
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.
References
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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