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Modes of Transmission

 

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Are you at risk? 1 in 50 Americans are infected with a virus called Hepatitis C

Click here to order a FREE Home Access Hepatitis C Test Kit.

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Hepatitis C is the most common liver disease currently seen in clinical practice. The incubation period, from the time of exposure to the virus until the onset of the disease, is one to six months

Q: How long after possible exposure to hepatitis C should you wait to be tested?

A: If you've had an accidental or other possible exposure to the hepatitis C virus, you should be screened for the hepatitis C antibody as soon as possible to determine your status at the time of the potential exposure. This is often called a "baseline" test and is used to determine whether a person already had antibodies to the hepatitis C virus at the time of a potential exposure to the virus.

After the exposure (especially if the blood exposure involved another person known to have the hepatitis C virus), it is recommended that testing for the hepatitis C antibody be performed at 4 to 6 months after the exposure OR that testing for the hepatitis C virus itself (a test often called an HCV PCR or hepatitis C viral load test) be performed 4 to 6 weeks after the potential exposure. These tests are done to determine whether or not hepatitis C infection has occurred as a result of the exposure.

Talk with your doctor to determine the appropriate follow-up testing that best suits your situation and needs.

http://www.hepcchallenge.org/doctalkquestion.php?category_id=7&keywords=&verbose_mode__keyword_search=Search

 

The virus is transmitted primarily by blood and blood products. The majority of infected individuals have either received blood transfusions prior to 1990 (when screening of the blood supply for HCV was implemented) or have used intravenous drugs.

Sexual transmission between monogamous couples is rare but HCV infection is more common in sexually promiscuous individuals. Perinatal transmission from mother to fetus or infant is also relatively low but possible (less than 10%). Many individuals infected with HCV have no obvious risk factors. Most of these persons have probably been inadvertently exposed to contaminated blood or blood products.

 

 

Myths of Hepatitis C Transmission

Like many common diseases, HCV is often misunderstood, and a number of myths have developed about how the disease is spread. Contrary to what you may have heard, hep C is not transmitted by:

Sneezing
Coughing
Hugging
Contaminated food or water
Sharing dishes, glasses or eating utensils
Casual contact.

How can you protect yourself from getting hepatitis C?

Unlike hepatitis B, there is no vaccine protective against hepatitis C (the HBV vaccine provides no protection against HCV), and prior infection with HCV does not protect against future infections as is the case with HBV.

To reduce your risk of becoming infected with hepatitis C:

• Avoid sharing needles, IV drugs, and drug paraphernalia
  Avoid skin piercing or tattoos
  Practice standard precautions if you are a health care worker
  Use care when handling any items that may have HCV-infected blood on them (such as razors, toothbrushes, nail clippers, sanitary napkins, and tampons)

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Household Contact

Can Hepatitis C Be Transmitted by Sharing Toothbrushes?

Study Links HCV, Tattoos

Intranasal Transmission of Hepatitis C Virus: Virological and Clinical Evidence

Needle Stick Exposure and Hepatitis C

Reducing Risk Of Vertical Hepatitis C Transmission

Hepatitis C in pregnancy

Mother-to-Child HCV Transmission

Prevention of Spread of HCV

Intranasal Transmission of Hepatitis C Virus: Virological and Clinical Evidence

Transfusions & Transplants

Methods of transmission

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HCV Sexual Transmission/Prevention From HCV Advocate

 Mother-to-Child Transmission
 Sexual Transmission of Hepatitis C
 Tattoos

March 09

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Transfusions & T

Risk Factors for Hepatitis C in People with Unknown Transmission Routes

 

FREE Home Access Hepatitis C Test Kit.

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Found elsewhere on our site

Sex and HCV

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Household Contact

Case-control studies also have reported an association between non-sexual household contact and acquiring hepatitis C. The presumed mechanism of transmission is direct or inapparent percutaneous or permucosal exposure to infectious blood or body fluids containing blood. In a recent investigation in the United States, an HCV-infected mother transmitted HCV to her hemophilic child during performance of home infusion therapy, presumably when she had an unintentional needle stick, and subsequently used the contaminated needle in the child.

Although prevalence of HCV infection among nonsexual household contacts of persons with chronic HCV infection in the United States is unknown, HCV transmission to such contacts is probably uncommon. In studies from other countries of nonsexual household contacts of patients with chronic hepatitis C, average anti- HCV prevalence was 4%. Although infected contacts in these studies reported no other commonly recognized risk factors for hepatitis C, most of these studies were done in countries where exposures commonly experienced in the past from contaminated equipment used in traditional and nontraditional medical procedures might have contributed to clustering of HCV infections in families.

 

Transmission of Hepatitis C among Family Members in Egypt

A study published in the current issue of Hepatology (September 2005) examines the incidence and risk factors associated with Hepatitis C virus (HCV) infection in rural Egypt..

The prevalence of antibodies to Hepatitis C Virus (HCV) in Egypt is among the highest in the world. From the 1950s until 1982 hundreds of thousands were infected during mass campaigns to control schistosomiasis (a parasitic disease) using mass therapy with intravenous antimony compounds, but little is known about current risk factors and rates of transmission. Studies of high risk populations, such as intravenous drug users, shed little light on HCV transmission in Egypt where this high risk behavior is rare.

In a study led by G. Thomas Strickland, M.D. of the Department of Epidemiology and Preventive Medicine at the University of Maryland School of Medicine in Baltimore, MD, Egyptian and American researchers surveyed rates of HCV infection in two rural communities having a prevalence of antibody to HCV of 24 and 9 percent.

A total of 10,112 HCV negative individuals were identified during an annual survey in 1997, with follow-up performed on an average of 1.6 years later in 6,738 subjects. Of these, 33 developed HCV antibodies, an incidence of 3.1/1000 person-years (PY), and 6.8/1000 PY in the 28 subjects in the village having the 24 percent prevalence of HCV. None of the 33 individuals was diagnosed with viral hepatitis or reported symptoms of acute hepatitis.

An analysis of risk factors showed the strongest predictor of infection with HCV was having an anti-HCV positive family member [emphasis added-Ed] Among those that did, incidence was 5.8/1000 PY, compared to 1.0/1000 PY; 27/33 incident cases had an anti-HCV positive family member. Parenteral exposures increased the risk of HCV, but were not statistically significant; 67 percent of seroconverters were less than 20 years old, and the highest incidence rate (14.1/1000 PY) was in children under 10 living in households with an anti-HCV positive parent in the village with the high prevalence of HCV antibodies. The infection rate was also increased (13.1/1000 PY) in men married to an HCV positive woman.

"We believe HCV exposures in rural Egyptian communities are usually less intense than those in individuals infected by contaminated blood, either from transfusion of blood or a blood product, or from abuse of intravenous drugs," the authors state.

Although not statistically proven to be a risk in this study, they cite frequent injections, usually given at home for health purposes with syringes and needles sometimes used for more than one person, as the most common parenteral exposure route. The strong relationship between the risk of infection in children and the presence of HCV antibodies in their parents suggests that transmission of HCV is occurring between family members, possibly by exposure to infectious blood or saliva, or by sharing needles.

In the past, mass treatment campaigns for schistosomiasis involving multiple injections may have caused numerous HCV infections in families, but this would not account for current infection rates, other than placing younger members of families living with those who contracted HCV in this way at higher risk.

The authors conclude: "It is exceedingly important to learn the mechanisms by which HCV transmission is occurring between family members so that preventive measures can be initiated, particularly in children having HCV-infected parents."

08/24/05

Reference
G T Strickland and others. Intrafamilial Transmission of Hepatitis C in Egypt. Hepatology 42(3): 683-87. September 2005. Article is available via Wiley InterScience

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Can Hepatitis C Be Transmitted by Sharing Toothbrushes?

Guidelines for the prevention of hepatitis C virus (HCV) transmission often include a warning against sharing toothbrushes, razors, nail care equipment, and other personal items that potentially may come into contact with blood. While studies definitively show that HCV can be transmitted by sharing needles and other equipment used for drug injection, the risk of sharing personal care articles is less clear.

German researchers performed a study to examine whether toothbrushes of HCV positive people are likely to be contaminated with the virus. The study included 30 participants with chronic hepatitis C. For each, 2 mL of saliva, collected before and after tooth brushing, plus toothbrush rinse water were tested for HCV RNA.

Results

Saliva collected before tooth brushing was positive for HCV RNA in 9 patients (30%).

Saliva collected after brushing the teeth had detectable HCV in 11 patients (36.7%).

12 toothbrush rinse water specimens (40%) tested positive for HCV RNA.

In 6 of these 12 patients, the "native" saliva (taken from the mouth) had been negative for HCV RNA.

Patients with detectable HCV RNA in their toothbrush rinse water showed no significant differences from those with negative rinse water with respect to clinical, biochemical, and virological parameters.

Conclusion

In conclusion, the authors wrote, "Our study demonstrates a contamination with HCV RNA of a considerable portion of toothbrushes used by hepatitis C patients, suggesting at least a theoretical risk of infection by sharing these objects."

They added that these results support "strengthening the recommendations to [ensure] a clear separation of these personal care objects between patients and their household members."

09/01/06

Reference
G Lock, M Dirscherl, F Obermeier, and others. Hepatitis C contamination of toothbrushes: myth or reality? Journal of Viral Hepatitis 13(9): 571-573. September 2006.

 

Tattoo and HCV

NEW YORK – Anyone with a tattoo should be tested for hepatitis C, according to researchers who conducted a recent study in New York.

The researchers studied 3,871 people, according to a report on medical-news.net, and found that patients with HCV were more likely to have had one or more tattoos. This was true and even after the data were adjusted for age, gender and ethnicity. When patients with the most common risk factors for HCV, injection drug use and blood transfusion prior to 1992, were removed, patients with HCV were about three times more likely to have had tattoos.

Nov. 1, 2007

Intranasal Transmission of Hepatitis C Virus: Virological and Clinical Evidence
	Clinical Infectious Diseases Oct 1 2008;47:931-934   Sagiv Aaron,1 James M. McMahon,2,5 Danielle Milano,3 Leilani Torres,2 Michael Clatts,7 Stephanie Tortu,6 Donna Mildvan,4 and Malgorzata Simm1   1Molecular Virology Division, St. Luke's-Roosevelt Institute for Health Sciences/Columbia University, 2National Development and Research Institutes, 3Boriken Neighborhood Health Center, and 4Division of Infectious Diseases, Beth Israel Medical Center, New York, and 5School of Nursing, University of Rochester Medical Center, Rochester, New York; 6School of Public Health, Louisiana State University, New Orleans; and 7School of Public Health, Center for Global Health Research, University of Puerto Rico, San Juan   "Our findings revealed a high prevalence of blood (74%) in the nasal secretions of HCV-positive long-term drug sniffers. We also confirmed that HCV RNA was present in the nasal secretions of a substantial proportion (13%) of this cohort. Most significantly, this study demonstrated that both blood and HCV particles can be transferred onto sniffing implements (i.e., straws) during simulated intranasal drug use."   ABSTRACT   Intranasal transmission of hepatitis C virus (HCV) via contaminated drug-sniffing implements is a potential but unconfirmed source of viral infection. We demonstrate the virological plausibility of intranasal transmission by confirming that blood and HCV RNA are present in the nasal secretions and drug-sniffing implements of HCV-infected intranasal drug users recruited from a community health clinic in New York City.   Hepatitis C virus (HCV) is the most common bloodborne pathogen in the United States and is a major cause of liver-related morbidity, mortality, and liver transplantation [1]. HCV is transmitted through contact with infected blood [2] (mostly via shared needles and other drug injection paraphernalia); however, a large proportion (up to 20%) of HCV infections remain unexplained, especially among noninjection drug users [3]. One hypothesis to account for these unexplained cases involves intranasal transmission of HCV via contaminated implements, such as straws, used to snort cocaine, heroin, and other powdered drugs [4]. Implements inserted into the nasal cavity, which has been eroded by long-term drug sniffing, might come into contact with HCV-infected mucus or blood, which might then be transmitted to a susceptible individual sharing the same implement [5]. Epidemiological studies of intranasal transmission of HCV have produced inconsistent findings [6, 7], in part because of the high correlation between drug sniffing and other risk factors for HCV infection. Here, we attempt to refute the intranasal transmission hypothesis by invalidating >1 of its virological preconditions. Specifically, we address 2 primary research questions: (1) Does HCV RNA exist in the nasal secretions of serum-positive drug sniffers? (2) If so, can HCV RNA be transferred onto the sniffing implements shared by intranasal drug users. A secondary aim was to examine clinical nasal pathologies that might facilitate intranasal HCV transmission.   Methods.   Our sample included low-income, urban intranasal drug users with chronic, active HCV infection. Subjects were primarily Hispanic and African American and were recruited from a neighborhood health clinic in East Harlem, New York City, an area with a high prevalence of HCV infection (up to 29%) among noninjection drug users [3]. Eligibility criteria included (1) age, 18 years; (2) self-reported intranasal drug use; and (3) a positive result of a quantitative HCV PCR blood test. Overall, 38 patients enrolled in the study and provided informed consent. Study protocols were approved by 3 institutional review boards.   The following medical information was obtained from subjects: quantitative HCV RNA test result and viral load, hepatitis B antibody test results, liver enzyme levels (i.e., alanine aminotransferase level), and liver biopsy history. Subjects completed a brief survey, in either Spanish or English, that covered demographic characteristics, risk factors for HCV infection, injection and noninjection drug use, health status, and nasal pathology symptoms.   Blood samples were collected for quantitative PCR. Two nasal secretion samples (1 from each nostril) were collected with Dacron nasal swabs and placed in (1) 1 mL of TRIzol reagent (Gibco BRL) for RNA detection or (2) 1 mL of OBTI solution for blood detection. Similarly, 2 experimental sniffing implements, which consisted of new (packaged) soda straws commonly used by drug sniffers, were collected from each subject. To avoid harmful effects of sniffing powdered substances, subjects were instructed to �gsnort air�h while mimicking their normal drug-sniffing behavior.   HCV RNA was isolated from 200 _L of serum by use of the QIAamp MinElute kit (Qiagen); HCV RNA was isolated from nasal secretions and sniffing implements using the TRIzol (Gibco BRL) on the basis of established protocols [8]. The first strand of cDNA was synthesized by ImProm-IITM Reverse Transcription System (Promega) using gene-specific downstream primers targeting the HCV p22 core region, with minor modification of the upstream primer (410R-5'-ATGTACCCCATGAGGTCGGC-3'). HCV cDNA was amplified by PCR with 40 cycles of denaturation (94�‹C for 30 s), annealing (58�‹C for 30 s), and elongation (72�‹C for 45 s) with primers 406F-5'-TAGACCGTGCACCATGAGC-3' and 410R. PCR products were detected by Southern blot using 32P-labeled probe (5'-AGGAAGACTTCCGAGCGGTCGCAA-3').   HCV cDNA was amplified from randomly selected HCV-positive blood samples with use of high-fidelity Pfu polymerase (Perkin Elmer) using 410R and 406F primers and cloned into a TA cloning vector (Invitrogen). The pTA_HCV was used to prepare standard curves ranging from 1 x 10-6th to 10 copies of HCV mRNA, which were run in parallel to each set of samples. The intensity of DNA bands was evaluated by densitometry using the Kodak Image Analysis System; the HCV load for the test sample was calculated on the basis of the numeric value derived from the HCV titration curve. HCV load was calculated as the number of copies per milliliter for blood specimens and as the number of copies per sample for nasal secretions and implements.   Traces of blood in nasal secretions and sniffing implements were detected by Hexagon OBTI Kit (BLUESTAR Forensic). Titration curves were prepared using human hemoglobin (Sigma) in 2-fold dilutions ranging from 10 to 0.1 μg/mL. The concentration of blood in each sample was established by comparing the OBTI intensity between the sample and the hemoglobin titration curve.   Nasal cavity pathology was assessed for each patient by anterior nasal examination, rendering diagnoses on 8 nasal pathologies. Rhinitis was diagnosed on the basis of the classic symptoms of mucosal and nasal secretion appearance [9]. Rhinosinusitis was defined by symptomatic inflammation of the paranasal sinuses and nasal cavity [10].   Sample prevalences of HCV RNA and occult blood in nasal secretions and on sniffing implements were estimated. Ninety-five percent CIs were calculated around point estimates using the adjusted Wald method. Descriptive statistics were calculated for sample descriptors and measures of nasal pathology. Our limited sample size precluded statistical tests of significance (e.g., associations between virological and clinical variables).   Results.   All 38 patients had chronic, active hepatitis C. The serum HCV load ranged from 250 to 5,000,000 copies/mL (median, 5000 copies/mL). Recent liver biopsies had been performed for 6 patients; all indicated chronic liver disease, with stages ranging from 1 to 4. Recent alanine aminotransferase levels were available for 17 patients; the mean level (±SD) was 46.7 +/- 26.7 U/L (range, 16-118 U/L). Antibody screening revealed that 34% of subjects were positive for antibodies to HIV, and 45% were positive for antibodies to hepatitis B virus.   Trace amounts of blood were detected in 28 (74%) of 38 nasal secretion samples (range, 0.1-10 μg/mL) and on 3 (8%) of the 38 sniffing implements (range, 0.1-2 μg/mL). HCV RNA was detected in 5 nasal secretion samples (13%; HCV RNA level range, 10-100 copies/sample) and on 2 sniffing implements (5%; HCV RNA level, 50 and 100,000 copies/sample). Prevalence estimates suggest a wide discrepancy between the presence of blood (74%) and the presence of HCV RNA (13%) in the nasal secretion samples (table 1). Of the 5 HCV RNA-positive nasal secretion samples, only 3 had traces of occult blood; of the 28 samples containing occult blood, 25 were negative for HCV RNA (figure 1).   The prevalence of rhinitis in this cohort was high (71%) (table 2). In contrast, the prevalence of rhinosinusitis (11%) is consistent with that of the general population. More than 40% of subjects experienced rhinorrhea or nasal congestion at least once per week, 8% reported nose bleeds at least once per week, and 8% and 16% reported mucosal lesions and crusting, respectively. Approximately one-half of the subjects attributed these symptoms to intranasal drug use. Four persons (11%) were observed to have nasal septal perforations; 1 (3%) had a nasopalatal perforation; and 6 (16%) displayed symptoms of saddlenose deformation. These pathologies have been associated with advanced nasal cavity deterioration associated with chronic intranasal drug use [11].   Discussion.   Our findings revealed a high prevalence of blood (74%) in the nasal secretions of HCV-positive long-term drug sniffers. We also confirmed that HCV RNA was present in the nasal secretions of a substantial proportion (13%) of this cohort. Most significantly, this study demonstrated that both blood and HCV particles can be transferred onto sniffing implements (i.e., straws) during simulated intranasal drug use. Studies have shown that HCV can remain viable on environmental surfaces for up to 16 h, but little is know about the quantity of virus required for transmission [12]. The prevalences of HCV in the nasal secretions and on sniffing straws are likely conservative estimates. It is reasonable to assume that HCV will be present in the nasal secretions with greater frequency and quantity during episodes of active drug sniffing, which may exacerbate discharge of nasal fluids and blood.   Data in table 1 contradict the assumption that, in persons with HCV-positive serum specimens, detection of blood implies the presence of HCV. This discrepancy may be explained by 2 factors. First, the 2 assays (PCR and OBTI) were not performed on the same samples. Second, the OBTI assay for blood detects immune complexes between human hemoglobin (hHb) and monoclonal anti-hHb antibodies, which can occur even in the absence of viable cells. In contrast, PCR can only detect HCV RNA from intact particles. Therefore, the discrepancy between the high prevalence of occult blood and relatively low detection of HCV RNA in nasal secretions may be associated with the rapid deterioration of viral RNA in the nasal environment or the destruction of viral particles by mucosal immunity. If the viability of HCV particles in nasal secretions is moderated by nasal pathology or immunity, this might help explain conflicting epidemiological findings in which these moderating factors are not considered.   This study establishes the validity of 2 primary virological preconditions necessary for intranasal HCV transmission: (1) the presence of blood and HCV in the nasal secretions of intranasal drug users, and (2) the transference of blood and HCV from the nasal cavity onto sniffing implements, which are often shared by intranasal drug users. Moreover, the frequency and severity of nasal pathologies observed in this cohort might aggravate conditions that facilitate intranasal HCV transmission. Consequently, these findings lend important virological and clinical support to the intranasal HCV transmission hypothesis. In addition, detection of HCV in nasal secretions advances the debate regarding potential iatrogenic and nosocomial transmission of HCV in the context of ear, nose, and throat and related clinical practices. More research is needed to confirm intranasal transmission as a mode of viral infection and to determine its impact on the wider epidemic of HCV infection.

 

Needle Stick Exposure and Hepatitis C

By Nancy Reau, MD and Donald M. Jensen, MD

Hepatitis C virus (HCV) is a hepatitis virus transmitted through blood-to-blood exposure. Hepatitis C is commonly acquired through blood product transfusions (primarily before 1992), needle sharing (including acupuncture), tattooing, body-piercing, and even through sharing personal hygiene items. In as many as 10% of individuals transmission route cannot be explained.

What is my risk of acquiring hepatitis C from a needlestick?

Unlike hepatitis B virus, hepatitis C is not efficiently transmitted from a needlestick. The average rate of seroconversion (changing from hepatitis C antibody negative to hepatitis C antibody positive) after an occupational exposure to HCV positive blood is about 1.8%, but has ranged as high as 7-10% in some studies. This risk is highest with hollow-bore needles.

What can be done to prevent the transmission of hepatitis C?

There is currently no vaccine or immunoglobulin (IG) to protect against HCV transmission. Several studies evaluating the response to passive immunoglobulin found that high anti-HCV titer IG did not prevent transmission. This makes sense given that the rapid mutation rate of HCV allows the virus to escape from any protective antibody that may form during infection. Postexposure treatment with interferon, with or without ribavirin, is also confusing and controversial. At present, however, there is no recommendation for the use of antiviral therapy following needlestick exposure to an HCV-positive source.

What should I do if I’m exposed to HCV positive blood?

Currently, the best recommendation is to carefully monitor for laboratory abnormalities, signs and symptoms of acute hepatitis C infection. Acute hepatitis C is a difficult disease to study. This is due to the declining incidence of acute hepatitis C and the fact that most patients are not initially symptomatic. Given these limitations, a non-controlled study evaluating the response to a 24-week course of interferon alfa (Jaeckel et al.,: Treatment of Acute Hepatitis C with Interferon Alfa-2b. NEJM 2001;345:1452-1457) found that 98 percent of treated patients exhibited a sustained biochemical and virologic response 24 weeks after treatment of acute hepatitis C. These are exciting results, especially given that previous studies suggested that only 15-30% of individuals with acute infection recover without treatment.

Should we treat everyone with acute hepatitis C or exposure to hepatitis C? Before recommending any treatment, we should be sure that it is the best thing for the patient. Interferon is expensive and has many side effects, some of which could be life-threatening. The study was not controlled (i.e., there was not a group with acute hepatitis C that did not receive treatment). We know that 15-30% of patients exposed to hepatitis C will recover without any treatment. In addition, the patients in the study were symptomatic and often had jaundice. Previous investigations suggest that progression to chronic hepatitis C is much lower in young patients with jaundice, making it more likely that these individuals could have spontaneous clearance. The individuals in the study were not treated immediately after exposure, but rather months after they had symptoms. This would suggest that therapy could be delayed without adverse affects, allowing patients to spontaneously recover before prescribing an expensive and difficult to tolerate medication. But the number one reason that interferon therapy is not standard in acute infection is that we need more data to ensure that this is the most beneficial treatment to offer. Currently, the US public health service guidelines for management of HCV exposures include:

1. Baseline testing for anti-HCV and ALT activity
2. Follow-up testing at 4-6 months for anti-HCV and ALT activity or HCV RNA at 4-6 weeks
3. Exposed individuals should not donate blood, plasma, organs, tissue, or semen
4. Exposed person does not need to modify sexual practices or refrain from pregnancy or discontinue breast feeding
5. When HCV infection is confirmed early, the person should be referred for medical management to a specialist in this area
6. IG and anti-viral agents are not recommended

The 2002 NIH Consensus conference recommended that patients with acute hepatitis C were potential candidates for interferon therapy, but realized many questions remained unanswered, particularly: which patients with acute HCV should be treated, and when is the ideal time to start therapy?

 

Copyright February 2003 – Hepatitis C Support Project - All Rights Reserved. Permission to reprint is granted and encouraged with credit to the Hepatitis C Support Project.

Back to Medical Writers' Circle

http://www.hcvadvocate.org/hcsp/articles/Jensen.html

 

Also see :

Infection Control:
Hepatitis C
Issues and Answers for Health Care Workers

http://www.hivdent.org/infctl/hepatiti.htm

Reducing Risk Of Vertical Hepatitis C Transmission
A DGReview of :"Mother-to-child transmission of hepatitis C virus: evidence for preventable peripartum transmission"
Lancet

09/15/2000
By Mark Greener


Vertical transmission of hepatitis C virus (HCV) appears to occur predominantly around delivery, a new study suggests.

The study also suggested that elective caesarean section before membrane rupture may virtually eliminate the risk of vertical transmission.

The authors note that until this study, few papers examined the timing of vertical HCV transmission. Moreover, no intervention was known to reduce transmission rates.

The new study enrolled 441 mother-child pairs from the UK and Ireland and used Polymerase Chain Reaction (PCR) assays to measure levels of HCV RNA (viral load).

Half the uninfected children became HCV-antibody negative after eight months. This increased to 95 per cent after 13 months. The authors estimated PCR's sensitivity as "only" 22 per cent during the first month. However, PCR's sensitivity rose to 97 per cent after the first month. The assay's sensitivity was not age-related.

Overall, the vertical transmission rate was 6.7 per cent. However, the vertical transmission rate was 3.8 times higher in the 22 women who were co-infected with HIV compared to those infected with HCV alone, after the authors adjusted for confounding factors.

Only 59 women breastfed. However, breastfeeding did not appear to affect the likelihood of transmission.

The study revealed that delivery by elective caesarean section before membrane rupture may virtually eliminate the risk of vertical transmission compared to delivery either vaginally or by emergency caesarean section. After adjusting for other factors, the authors estimated the average odds ratio for the risk of vertical transmission among babies delivered by elective caesarean section as zero.

In conclusion, the authors highlighted two findings suggesting that vertical HCV transmission occurs mainly around delivery. PCR's low sensitivity soon after birth and the reduced risk of transmission following elective caesarean section.

The authors suggest reconsidering the value of antenatal HCV testing if further investigations confirm that elective caesarean section reduces the likelihood of vertical transmission.
 

Hepatitis C in pregnancy
 

Risk Factors for Mother-to-child Transmission of Hepatitis C Virus
 

By Liz Highleyman

Hepatitis C virus (HCV) infection in children is mainly acquired via mother-to-child (perinatal) transmission. In a study published in the August 20,2007 issue of AIDS, French researchers sought to identify risk factors for mother-to-child HCV transmission, in particular those associated with maternal virological characteristics or mode of delivery.

The investigators included 214 HCV positive women and their newborn infants seen at 6 hospitals in southern France between October 1998 and September 2002. About one-quarter (55%) of the women were HIV-HCV coinfected. The authors collected data on maternal characteristics, circumstances of delivery, and laboratory data for the mothers and children. All babies were followed for 1 year, and those with detectable plasma HCV RNA for 2 years.

Results

• In total, 12 infants had detectable HCV RNA at 1 year of age, yielding an overall mother-to-child transmission rate of 5.6%.

• 3 of these children became HCV RNA negative between 12 and 18 months of age and achieved normal alanine aminotransferase (ALT) levels.

• 137 women (69%) had detectable plasma HCV RNA, including all those whose children were infected.

• 6 children were born to HIV-HCV coinfected women with detectable HCV RNA, for a transmission rate of 13.6%.

• 6 were born to HCV monoinfected women with detectable HCV RNA, for a transmission rate of 6.5%.

• The risk of mother-to-child HCV transmission was 3 times higher for HCV-HIV coinfected women compared to those with HCV alone (P = 0.05).

• When maternal HCV RNA levels were below 6 log IU/ml, the rate of transmission was significantly higher in HIV-HCV coinfected women (odds ratio 8.3; P = 0.01.

• This association with HIV status did not exist, however, for women with detectable HCV RNA levels of 6 log IU/ml or higher.

• The rate of HCV transmission did not differ significantly between children born by vaginal delivery or Caesarean section after membrane rupture and those born by elective Caesarean section, independent of HIV status.

Conclusion

These findings confirm results of past studies showing that HIV-HCV coinfected women are more likely to transmit HCV to their babies than those with HCV alone. The study also confirmed that HCV viral load plays an important role in mother-to-child transmission/

Department of Public Health, France; CHU Nice, France; CHU Toulouse, France; CHU Montpellier, France; CHG Antibes, France; Virology Laboratory, France; INSERM U379, France.

08/21/07

Reference
E Marine-Barjoan, A Berrebi, V Giordanengo, and others (for the ALHICE study group). HCV/HIV co-infection, HCV viral load and mode of delivery: risk factors for mother-to-child transmission of hepatitis C virus? AIDS 21(13): 1811-1815. August 20, 2007.

http://www.hivandhepatitis.com/hep_c/news/2007/082107_a.html

 

Mother-to-Child HCV Transmission

2009

Women with chronic hepatitis C may transmit HCV to their babies during pregnancy or delivery. This is uncommon overall – occurring at a rate of about 5% – but is more likely when the mother is HIV positive. As reported in the December 1, 2008 Journal of Infectious Diseases, K. Dowd and colleagues studied 63 HIV/HCV coinfected pregnant women to assess whether lower levels of HCV-specific neutralizing antibodies are associated with an increased risk of mother-to-child HCV transmission. Sixteen women (25%) transmitted HCV to their infants. There was no significant difference between transmitting and non-transmitting mothers in terms of the ability of maternal plasma to neutralize HCV (median neutralizing antibody titers of 1:125 vs. 1:100, respectively). "In the setting of HIV/HCV coinfection, we found no evidence that HCV neutralizing antibodies are associated with the prevention of mother-to-child transmission of HCV," the researchers concluded.

http://www.hcvadvocate.org/news/newsRev/2009/HJR-6.1.html#5

Discordant Mother-to-Child Transmission of HCV in Twin Pregnancies

May 2007

 

Perinatal

The average rate of HCV infection among infants born to HCV-positive, HIV negative women is 5%-6% (range: 0%-25%), based on detection of anti-HCV and HCV RNA, respectively. The average infection rate for infants born to women co-infected with HCV and HIV is higher - 14% (range: 5%-36%) and 17%, based on detection of anti-HCV and HCV RNA, respectively. The only factor consistently found to be associated with transmission has been the presence of HCV RNA in the mother at the time of birth. Although two studies of infants born to HCV-positive, HIV-negative women reported an association with titer of HCV RNA, each study reported a different level of HCV RNA related to transmission. Studies of HCV/HIV-coinfected women more consistently have indicated an association between virus titer and the transmission of HCV.

The only consistent factor found to be associated with
HCV transmission during birth is the presence of HCV
 in the mother at the time of birth
 

Data regarding the relationship between delivery mode and HCV transmission are limited and presently indicate no difference in infection rates between infants delivered vaginally compared with cesarean-delivered infants. The transmission of HCV infection through breast milk has not been documented.  In the studies that have evaluated breastfeeding in infants born to HCV-infected women, the average rate of infection was 4% in both breastfed and bottle-fed infants.

Diagnostic criteria for perinatal HCV infection have not been established. Various anti-HCV patterns have been observed in both infected and uninfected infants of anti-HCV-positive mothers. Passively acquired maternal antibody might persist for some months, but probably not for >12 months. HCV RNA can be detected as early as 1 to 2 months.

Pregnancy and Breast feeding

Should pregnant women be routinely tested for anti-HCV?
No. Pregnant women have no greater risk of being infected with HCV then non-pregnant women. If pregnant women have risk factors for hepatitis C, they should be tested for anti-HCV.

What is the risk that HCV infected women will spread HCV to their newborn infants?
About 5 out of every 100 infants born to HCV infected women become infected. This occurs at the time of birth, and there is no treatment that can prevent this from happening. Most infants infected with HCV at the time of birth have no symptoms and do well during childhood. More studies are needed to find out if these children will have problems from the infection as they grow older. There are no licensed treatments or guidelines for the treatment of infants or children infected with HCV. Children with elevated ALT (liver enzyme) levels should be referred for evaluation to a specialist familiar with the management of children with HCV-related disease.

Should a woman with hepatitis C be advised against breast-feeding?
No. There is no evidence that breast-feeding spreads HCV. HCV-positive mothers should consider abstaining from breast-feeding if their nipples are cracked or bleeding.

When should babies born to mothers with hepatitis C be tested to see if they were infected at birth?
Children should not be tested for anti-HCV before 18 months of age as anti-HCV from the mother might last until this age. If diagnosis is desired prior to 18 months of age, testing for HCV RNA could be performed at or after an infant's first well-child visit at age 1-2 months. HCV RNA testing should then be repeated at a subsequent visit independent of the initial HCV RNA test result.

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Prevention of Spread of HCV

Miriam J. Alter, Ph.D.

Historically, the most reliable data on risk factors associated with acquiring hepatitis C virus (HCV) infection have been obtained from cohort (prospective) studies that determined the risk of developing acute infection after a specific exposure and case-control (retrospective) studies that determined if a history of exposure before onset of disease was associated with newly acquired (acute) hepatitis C. Risk factors identified by these studies in the United States included injecting drug use, blood transfusion and solid organ transplants from infected donors, occupational exposure to blood (primarily contaminated needle sticks), birth to an infected mother, sex with an infected partner, or multiple heterosexual partners.

The major limitation of such studies is that they are unlikely to identify associations with exposures that result only rarely in infections. For example, results of case-control studies have indicated no association between acquiring hepatitis C and exposures resulting from medical, surgical, or dental procedures. However, outbreaks of HCV infection have been associated with contaminated equipment in hemodialysis settings and unsafe injection practices in both inpatient and outpatient settings. Most of these outbreaks have involved patient-to-patient transmission. Only two instances of transmission have been reported from HCV-infected health care workers to patients in the United States. Neither of these was associated with the performance of exposure-prone invasive procedures, but rather with contamination of patients’ narcotics used for self-injection.

The contribution of these various risk factors to the overall burden of HCV infections is influenced both by their efficiency in transmitting HCV and by the frequency of the exposure in the population. In the United States, the relative importance of the two most efficient exposures associated with transmission of HCV, blood transfusion and injecting drug use, has changed over time. Blood transfusion, which accounted for a substantial proportion of HCV infections acquired >15–20 years ago, rarely accounts for recently acquired infections. In contrast, injecting drug use consistently has accounted for a substantial proportion of HCV infections and currently accounts for 60 percent of HCV transmission. The relative importance of other exposures has changed little over time.

Unprotected sex with an infected partner or with multiple partners has accounted for an estimated 15 percent of HCV infections. Although the role of sexual activity in the transmission of HCV remains controversial, and the virus is inefficiently spread in this manner, the relatively substantial contribution of sexual exposures to the burden of disease can be explained by the fact that sexual activity with multiple partners is a common behavior in the population and that the large number of chronically infected persons provides multiple opportunities for exposure.

In contrast to sexual exposures, occupational and perinatal exposures contribute to a small proportion overall of infections, and together with nosocomial or iatrogenic exposures, they account for about 5 percent of HCV infections. HCV is not transmitted efficiently through occupational exposure. The prevalence of HCV infection among health care or public safety workers averages 1–3 percent and has not been affected by changes or improvements in barrier precautions. Transmission rates from HCV infected mothers to their infants average 5 percent or less, no associations have been demonstrated with mode of delivery or type of feeding, and infants who acquire HCV infection at birth may be less likely to develop chronic infection.

Thus, about 90 percent of HCV infections can be accounted for by known percutaneous or mucosal exposures to blood. In the remaining 10 percent, no recognized source for infection can be identified. Numerous studies have attempted to identify additional risk factors for HCV infection. While case-control studies of acute hepatitis C reported no association with tattooing, acupuncture, ear piercing, military service, or foreign travel, cross-sectional and prevalence studies of volunteer blood donors, disease-specific clinic patients, and veterans receiving care in VA hospitals have yielded conflicting results for some of these risk factors. The lack of consistency among studies of highly selected groups for which the temporal sequence of exposure relative to the disease was unknown is cause for concern about the generalizability of such results.

Strategies for reducing or eliminating the potential risk for transmission include: (1) screening and testing of donors; (2) virus inactivation of plasma-derived products; (3) risk reduction counseling and services; and (4) implementation and maintenance of infection-control practices. Strategies for reducing risks for chronic disease include: (1) identification, counseling, and testing of at-risk persons; and (2) medical evaluation and management of infected persons.

Health care professionals in all patient care settings routinely should obtain a history that inquires about blood transfusion, use of illegal drugs (injection and non-injection) and evidence of high-risk sexual practices, such as multiple sex partners or history of STDs. Primary prevention of illegal drug injecting will eliminate the greatest risk factor for HCV infection in the United States. Although consistent data are lacking regarding the extent to which sexual activity contributes to HCV transmission, persons having multiple sex partners are at risk of STDs such as HIV, HBV, syphilis, gonorrhea, and chlamydia.

Testing should be offered routinely to persons most likely to be infected with HCV, which include persons who ever injected illegal drugs; received plasma-derived products known to transmit HCV infection that were not treated to inactivate viruses; received transfusions or solid organ transplants before July 1992; and were long-term hemodialysis patients. Based on a recognized exposure, testing also is indicated for health-care workers after needle sticks, sharps, or mucosal exposures to HCV-positive blood and for children born to HCV-positive women. Immune globulin and antiviral agents are not recommended for post-exposure prophylaxis of hepatitis C.

HCV-positive persons with a long-term steady partner do not need to change their sexual practices; however, they should discuss with their partner the need for counseling and testing, and the couple should be informed of available data on risk for sexual transmission of HCV to assist them in making decisions about precautions, including the low, but not absent, risk for transmission. HCV-positive persons do not need to avoid pregnancy or breastfeeding, and determining the need for cesarean delivery vs. vaginal delivery should not be made on the basis of HCV infection status. There are no recommendations for routine restriction of professional activities for HCV-infected health-care workers, and persons should not be excluded from work, school, play, child-care or other settings on the basis of their HCV infection status.

References

1. Centers for Disease Control and Prevention. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR 1998;47(No. RR-19):1–33.
2. Alter MJ, Kruszon-Moran D, Nainan OV, et al. Prevalence of hepatitis C virus infection in the United States. N Engl J Med 1999;341:556–62.
3. Polish LB, Tong MJ, Co RL, et al. Risk factors for hepatitis C virus infection among health care personnel in a community hospital. Am J Infect Control 1993;21:196–200.
4. Panlilio AL, Shapiro CN, Schable CA, et al. Serosurvey of human immunodeficiency virus, hepatitis B virus, and hepatitis C virus infection among hospital-based surgeons. J Am Coll Surg 1995;180:16–24.

 http://janis7hepc.com/hepatitis_c_research7.htm

 

Transfusions & Transplants

Currently, HCV is rarely transmitted by blood transfusion. During 1985-1990, cases of transfusion-associated non-A, non-B hepatitis declined by >50% because of screening policies that excluded donors with human immunodeficiency virus (HIV) infection and donors with surrogate markers for non-A, non-B hepatitis. By 1990, risk for transfusion-associated HCV infection was approximately 1.5% per recipient or approximately 0.2% per unit transfused. During May 1990, routine testing of donors for evidence of HCV infection was initiated, and during July 1992, more sensitive- multi-antigen- testing was implemented, reducing further the risk for infection to 0.001% per unit  transfused ( i.e.,1 in 100,000 per unit transfused).

Current risk for transfusion-associated hepatitis C is 1/100,000 per unit transfused.

Receipt of clotting factor concentrates prepared from plasma pools posed a high risk for HCV infection until effective procedures to inactivate viruses, including HCV, were introduced during 1985 (Factor VIII) and 1987 (Factor IX). Persons with hemophilia who were treated with products before inactivation of those products have prevalence rates of HCV infection as high as 90%. Although plasma derivatives (e.g., albumin and immune globulin (IG) for intramuscular (IM) administration) have not been associated with transmission of HCV infection in the United States, intravenous (IV) IG that was not virally inactivated was the source of one outbreak of hepatitis C during 1993-1994. Since December 1994, all IG products - IV and IM- commercially available in the United States must undergo an inactivation procedure or be negative for HCV RNA (ribonucleic acid) before release.

Transplantation of organs (e.g., heart, kidney, or liver) from infectious donors to the organ recipient also carried a high risk for transmitting HCV infection before donor screening. Limited studies of recipients of transplanted tissue have implicated transmission of HCV only from nonirradiated bone tissue of unscreened donors. As with blood donor screening, use of anti-HCV (antibody to hepatitis C virus)- negative organ and tissue donors has virtually eliminated risks for HCV transmission from transplantation

http://www.cdc.gov/ncidod/diseases/hepatitis/c_training/edu/1/epidem-trans-2.htm

 

	Sex and HCV