The prevalence of HCV in Egypt is strongly age-related, with older persons having prevalence greater than 50% in some regions. Tom Strickland has been a major contributor to understanding this epidemic, and summarizes the story here: http://www.ncbi.nlm.nih.gov/pubmed/16628669 - with the short answer being unsafe injection practices (non-sterile needles). The most intense exposure at the population level was an effort to treat schistosomiasis, during which injections were given very rapidly to large numbers of people in the Nile river delta, as described by Christina Frank and others (including Strickland) here: http://www.ncbi.nlm.nih.gov/pubmed/10752705

With others I helped characterize the genetic epidemiology in this report: http://www.ncbi.nlm.nih.gov/pubmed/10950762. Oliver Pybus and others performed phylodynamic analysis of the Egyptian HCV epidemic: http://www.ncbi.nlm.nih.gov/pubmed/12644558

The prevalence of HCV in Egypt is strongly age-related, with older persons having prevalence greater than 50% in some regions. Tom Strickland has been a major contributor to understanding this epidemic, and summarizes the story here: http://www.ncbi.nlm.nih.gov/pubmed/16628669 - with the short answer being unsafe injection practices (non-sterile needles). The most intense exposure at the population level was an effort to treat schistosomiasis, during which injections were given very rapidly to large numbers of people in the Nile river delta, as described by Christina Frank and others (including Strickland) here: http://www.ncbi.nlm.nih.gov/pubmed/10752705

With others I helped characterize the genetic epidemiology in this report: http://www.ncbi.nlm.nih.gov/pubmed/10950762. Oliver Pybus and others performed phylodynamic analysis of the Egyptian HCV epidemic: http://www.ncbi.nlm.nih.gov/pubmed/12644558

The high incidence of HCV in Egypt is quite intriguing. The high prevalence in children points to vertical transmission.

Similar to other blood-borne pathogens, hepatitis C virus (HCV) can be transmitted from an infected mother to her child in the perinatal period (vertical transmission). When no preventive measures are taken to prevent transmission of HCV, human immunodeficiency virus (HIV), or hepatitis B virus (HBV), vertical transmission of HCV occurs relatively less frequently than with HIV or HBV. Reported estimates of perinatal HCV transmission range from 0 to 44%, with larger studies indicating a vertical transmission risk in the 4 to 10% range

Risk Factors for Perinatal HCV Transmission

The risk of HCV transmission to infants appears to increase with detectable hepatitis C viremia during pregnancy[2,5,6,8,9,10,11,12 ]

Route and Timing of Perinatal HCV Transmission

The precise mechanism of vertical HCV transmission remains unclear, but infection appears to predominantly occur in utero or intrapartum, and not by breastfeeding. Long-term follow-up of HCV vertically infected infants and children has shown that a small proportion of neonates have hepatitis C viremia in the first month of life, whereas most do not become viremic until three or more months post-partum, thus suggesting intrapartum infection is more common than in utero infection[2,7,8,9,10,12 ]. Hepatitis C viral RNA has been detected in peripheral blood mononuclear cells, amniotic fluid, and vaginal secretions of chronically HCV-infected women and in cord blood of infected and noninfected neonates[12 ]. One study has suggested that HCV RNA detected in vaginal secretions represents the presence of non-viable viral particles, which may explain the relatively low rate of sexual and vertical transmission of HCV when compared with other blood borne pathogens[23]. As noted above, transmission of HCV through breast milk does not appear to be a significant source of infection, as demonstrated by the multiple transmission studies in which a proportion of HIV-uninfected women breastfed their neonates; in addition, several of these studies reported low rates of HCV RNA detection in breast milk[3,12]. Zanetti AR, Tanzi E, Paccagnini S, et al. Mother-to-infant transmission of hepatitis C virus. Lombardy Study Group on Vertical HCV Transmission. Lancet. 1995;345:289-91.

1. Polywka S, Feucht H, Zollner B, Laufs R. Hepatitis C virus infection in pregnancy and the risk of mother-to-child transmission. Eur J Clin Microbiol Infect Dis. 1997;16:121-4.

2. Tovo PA, Palomba E, Ferraris G, Principi N, Ruga E, Dallacasa P, Maccabruni A. Increased risk of maternal-infant hepatitis C virus transmission for women coinfected with human immunodeficiency virus type 1. Italian Study Group for HCV Infection in Children. Clin Infect Dis. 1997;25:1121-4.

[

3. Granovsky MO, Minkoff HL, Tess BH, et al. Hepatitis C virus infection in the mothers and infants cohort study. Pediatrics. 1998;102:355-9.

4. Thomas DL, Villano SA, Riester KA, et al. Perinatal transmission of hepatitis C virus from human immunodeficiency virus type 1-infected mothers. Women and Infants Transmission Study. J Infect Dis. 1998;177:1480-8.

[

5. Conte D, Fraquelli M, Prati D, Colucci A, Minola E. Prevalence and clinical course of chronic hepatitis C virus (HCV) infection and rate of HCV vertical transmission in a cohort of 15,250 pregnant women. Hepatology. 2000;31:751-5.

[

6. Ruiz-Extremera A, Salmeron J, Torres C, et al. Follow-up of transmission of hepatitis C to babies of human immunodeficiency virus-negative women: the role of breast-feeding in transmission. Pediatr Infect Dis J. 2000;19:511-6.

7. Ceci O, Margiotta M, Marello F, et al. Vertical transmission of hepatitis C virus in a cohort of 2,447 HIV-seronegative pregnant women: a 24-month prospective study. J Pediatr Gastroenterol Nutr. 2001;33:570-5.

8. Resti M, Bortolotti F, Vajro P, Maggiore G; Committee of Hepatology of the Italian Society of Pediatric Gastroenterology and Hepatology. Guidelines for the screening and follow-up of infants born to anti-HCV positive mothers. Dig Liver Dis. 2003;35:453-7.

[

9. Ferrero S, Lungaro P, Bruzzone BM, Gotta C, Bentivoglio G, Ragni N. Prospective study of mother-to-infant transmission of hepatitis C virus: a 10-yearsurvey (1990-2000). Acta Obstet Gynecol Scand. 2003;82:229-34.

10. Mast EE, Hwang LY, Seto DS, Nolte FS, Nainan OV, Wurtzel H, Alter MJ. Risk factors for perinatal transmission of hepatitis C virus (HCV) and the natural history of HCV infection acquired in infancy. J Infect Dis. 2005;192:1880-9.

[

11. European Paediatric Hepatitis C Virus Network. A significant sex-but not elective cesarean section-effect on mother-to-child transmission of hepatitis C virus infection. J Infect Dis. 2005;192:1872-9.

[

12. Marine-Barjoan E, Berrebi A, Giordanengo V, et al. HCV/HIV co-infection, HCV viral load and mode of delivery: risk factors for mother-to-child transmission of hepatitis C virus? AIDS. 2007;21:1811-5.

Most of the literature has attributed the high incident rate of HCV infection among Egyptians to the hygiene. Historically, there is a story spread in literature that is when Egyptians built the High Dam in Aswan(1950s), Nile river's flora has been affected. This leads to higher incident rate of Schistosomiasis among Egyptians. Assuming that among Schistosomiasis are HCV infected subjects and assuming also that those subjects used the same HCV contaminated injection needles. This leads to HCV infection became an endemic among Egytpians. I do not believe this story. An hypothesis that needs to be tested is that HCV genotype 4 is uniquely adopted to replicate in an arthropod. This hypothetical arthropod is responsible for the higher rate of infection among Egyptians.

Adel Nour: (i) The phylodynamic analyses for HCV match the epidemic history of the schistosomiasis treatment campaign. (ii) There is no evidence that HCV can replicate, or be transmitted by, any arthropod. (iii) The rate of spread of HCV in Egypt has slowed considerably since the schistosomiasis treatment campaign ended (with big drops in HCV prevalence among younger people compared with those who received injections for schistosomiasis). Thus, the arthropod conjecture does not fit available evidence, whereas the needle campaign fully fits. I think your proposal would be a waste of precious resources.

Stuart Ray: 1-The schistosomesis treatment compaign in Egypt is now past however, the incident rate of HCV genotype 4 is still very high among Egyptian. 2-can please cite the study that described that phylodynamic analysis of HCV matched the epidemic of schistosomiasis treatment campaign? 3-I do understand that there is no single study showed that HCV can replicate in an arthropod; it is simply an alternative hypothesis.

an update to my previous reply:

I found an old paper published by Germi R, et al., 2001 in Journal of medical virology showed that HCV binds and replicates in mosquito cells. Though this is not an evidence that the virus is transmitted via Mosquatos however, it at least proved that no host restriction factor prevents the virus to replicate in certain Mosquato cells. Mosquotos are already known to transmitted closely related HCV viruses such as Yellow fever and Dengue viruses. So far no single direct evidence supports the transmission of HCV via mosquotos or other arthropods however, it is very interesting hypothesis to test especially in nations with very high incident rate of HCV infection and diverse arthropods such as Egypt.

The Germi 2001 study was entirely in vitro. There is no evidence that HCV replicates within mosquitoes (and epidemiologic evidence does not provide support for arthropod transmission). Dengue and Yellow Fever Virus are arboviruses and members of the flavivirus genus; HCV is neither. While the hepacivirus genus and the flavivirus genus belong to the Flaviviridae family, they are very distantly related. While your speculation about insect transmission of HCV is interesting, it is neither novel nor necessary to explain what we know about HCV epidemiology. I won't claim to prove the negative; I just see no need to focus on a hypothesis that has been investigated fruitlessly before. Let's focus on reducing the continued spread of HCV by unsafe medical practices and injection drug use, both of which are known to continue.

You may also want to consider other situations such as in aboriginal populations of North America: See an interesting report distinguishing sero prevalence and virememia among First nation Indian

Can J Gastroenterol. 2003 Dec;17(12):707-12.

Viral hepatitis in the Canadian Inuit and First Nations populations.

Minuk GY1, Uhanova J.

Abstract

OBJECTIVE:

To review published prevalence data regarding hepatitis A (HAV), B (HBV) and C (HCV) in Canadian Inuit and First Nations populations.

METHODS:

PubMed database search and review of all papers describing data derived from seroepidemiological surveys.

RESULTS:

The prevalence of anti-HAV positivity in Canadian Inuit and First Nations populations reported to date is high (range 75% to 95%) and approximately three times that of non-Aboriginal Canadians residing in the same communities. Among the Canadian Inuit, the prevalence of HBV infection is approximately 5%, or 20 times that of non-Aboriginal Canadians, while the risk of exposure to HBV is 25%, or five times higher. Regarding the First Nations population, preliminary data suggest the prevalences of HBV infection (0.3% to 3%) and exposure (10% to 22%) are similar to rates in non-Aboriginals residing in the same regions and participating in similar high risk activities. Serological evidence of HCV infection (anti-HCV) is more common in the Canadian Inuit and First Nations (1% to 18%) than the remainder of the Canadian population (0.5% to 2%); however, viremia (HCV-RNA positivity) is less common (less than 5% versus 75% of anti-HCV positive individuals, respectively).

CONCLUSIONS:

Viral hepatitis is common in the Canadian Inuit and First Nations populations. In the absence of coexisting human immunodeficiency virus infection and alcohol abuse, the outcomes of HBV and HCV appear to be more benign than in non-Aboriginal Canadians

Bottom line:

While evaluating the prevalence of HCV, one need to address both exposure[antibody response] and viremia [viral RNA in circulation]

Being a highly endemic population, other routes of Transmission may be highly favorable such as, iatrogenic transmission and blood transfusion related transmissions . many reports have addressed this already.

A-study of mine established a strong correlation between Hcv infections in Gaza and undergoing any medical procedure in Egypt. Hcv infected people who had been previously referred to Egyptian hospitals for surgical procedures have genotype 4 the Common one in Egypt . On the other hand those who Underwent such surgeries locally or in other countries have genotype 1 .

Refference;

Most common genotypes and risk factors for HCV in Gaza strip: a cross sectional study

Basim M Ayesh12*, Sofia S Zourob3, Salah Y Abu-Jadallah2 and Yonat Shemer-Avni4

Hi, Thank you for the interesting question.

As highlighted above, HCV prevalence in Egypt was mainly due to mass vaccination practices in the 60's, when same needles were used. At the time, HepC was not discovered as yet. 

I have also once come across an article describing a similar situation in YEMEN. It was also reportedly due to Egyptian aid workers offering mass vaccination in certain areas of the Yemen (again 60's?). I think it could be postulated that it was the first iatrogenic outbreak of hep C at the time... I would appreciate it, if anyone has a link to such article.

The spread of HCV in Egypt is linked to anti-bilharziasis campaigns

The prevalence of liver disease in Egypt is high. It is mainly due to HCV and approximately 20% of the population has antibodies to HCV. Most infected people have participated in campaigns for the treatment of bilharziasis  in the 80s. Bilharziasis is caused by the presence of trematode worms of the genus Schistosomia in blood vessels. To fight against this infection, intravenous injection of emetic tartrate (parenteral antischistosomal therapy or PAT) was widely practiced between 1960 and 1980.

 As published, (Lancet, 2000), the scientists therefore believe that the administration of emetic tartrate  played a major role in the spread of HCV in Egypt. The needles used in the chain were improperly sterilized and entire villages have been thus contaminated. This led to the formation of a large reservoir of infection among the adult population, which explains the high prevalence of HCV and therefore the risk of high transmission.

Could we be missing a trick here in countries with endemic HCV infection?

Endemic HCV appears to be concentrated in the tropics and sub-tropics. Human populations in these regions experience higher biting rates due to an abundance of many varieties of arthropods. The rest of the human pathogenic flaviviruses are vector borne and HCV has been isolated from bodies or heads of mosquitoes collected from the houses of HCV-infected individuals (Chang et al 2001, Hassan et al 2003). Prof Oliver Pybus writes extensively on this subject suggesting the possibility of arthropod transmission of HCV (Pybus 2009).

West Nile virus is an infection caused by a Flavivirus. The animal reservoir of the virus consists of birds and its vector is a mosquito of the Culex genus. The disease initially affected Africa, part of central and southern Europe, the Middle East, and India but is spreading to the West. It remains to be seen if co-infection of insect-specific flaviviruses will change the vector competence of mosquitoes for pathogenic flaviviruses (Huang et al 2014; Huhtamo, et al 2014).

When a mosquito bites, it injects saliva through one channel. The saliva functions as a lubricant to help the mosquito feed easier. The blood that a mosquito sucks as a meal flows in a completely separate tube than the channel that saliva is injected and only in one direction: towards the mosquito. So, it's biologically unlikely for infected blood to be spread to another person when the insect feeds off an uninfected individual. Biological transmission occurs when the disease agent replicates or develops within the fly prior to transmission as is the case with Malaria (Anopheles) and this is considered not to happen with HCV virions in mosquitoes (WHO). Thus it is understood that infected blood from one person is not injected into another human causing HCV infection. However, mechanical transmission occurs when the disease agent is transmitted without amplification and development within the fly via contaminated blood remaining on the insect’s mouthparts (Mullens, 2002, Baldacchino et al 2014). HCV can survive outside the body for 4 days and is difficult to destroy, except by autoclaving. Therefore, HCV may remain infectious on the proboscis of an arthropod for a period of time, enabling it to infect the next mammal that it feeds from. Hepatitis C virus RNA was detected in the heads of symbiotic mosquitoes collected from homes of HCV positive patients at 3h and 6h after feeding (Hassan et al, 2003).

Annwyne's post is interesting but contains multiple flaws. For one, HCV is not a flavivirus (it is a member of the Flaviviridae family, but not the Flavivirus genus). HCV is a hepacivirus, and there is no evidence for transmission of any member of the hepaciviruses (primate or other) by arthropod. It's been raised as she notes, but the epidemiology does not support it - the spread of HCV in countries like Egypt is explicable by things like unsafe injection practices. HCV is not "difficult to destroy" - it is rendered noninfectious by weak detergent and a variety of other means.  While an interesting hypothesis, there's precious little to support arthropod transmission of HCV.

Thank you, Stuart, so much for your comments and I really value your interest in the post. I wish to raise awareness and consideration of this hypothesis for discussion. I prefer to consider the comparison between hepacivirus and flavivirus as more of an academic lateral jump than a 'flaw' but I do take the point. This vehicle for discussion is such an engaging space for musing on new concepts, blue sky thinking and ‘thinking aloud’. So thanks again for engaging with the subject.

The iatrogenic transmission that occurred in the 1930s–1950s during a period that coincided with targeted extensive antischistosomal injection campaigns using HCV infected injection equipment could have been avoided by their efforts to clean the injecting equipment if HCV was so easy to neutralise.

It is clear that biological transmission is generally considered to be the most important mechanism for arthropod transmission of other viral infections and has been dismissed as a vehicle for HCV transmission but mechanical transmission is possibly worth consideration as there is evidence of HCV survival on the proboscis of an arthropod where HCV may remain infectious on the proboscis of an arthropod for a period of time, enabling it to infect the next mammal that it feeds from (Hassan et al, 2003).

Mechanical transmission occurs when the disease agent is transmitted without amplification and development within the fly via contaminated blood remaining on the insect’s mouthparts (Mullens, 2002, Baldacchino et al 2014). It has been thought that mechanical transmission is of minor epidemiological importance for transmitting diseases and that biological vectors carry much more relevance with this regard (Cam et al, 1996). However, although the impact of this is difficult to assess, in specific circumstances, mechanical transmission can be an efficient way of transmitting an infection and as effective as biological transmission. Probability of transmission can increase as to the immediate circumstances and conditions at the time (Desquesnes et al., 2009). There are several factors that can enhance mechanical transmission including interrupted feeding, quantity of blood meal residues on mouthparts, sensitivity to host defensive reactions and the tendency to switch hosts, biting intensity and quantity (Desquesnes et al., 2009). Other factors include, high levels of microbes in the vector, frequent biting and the close proximity and contact between vectors and recipients and high density of insects. In Egypt there is a high density of HCV infection and a comparatively high density of biting insects giving a high proximity of infected individuals. Much discussion so far on tis subject has involved nonhuman subjects and again relating this to human subjects may be an interesting exercise.

Some references in support

Germi R1, Crance JM, Garin D, Guimet J, Thelu MA, Jouan A, Zarski JP, Drouet E. Mosquito cells bind and replicate hepatitis C virus. J Med Virol;64(1):6-12. 2001

Desquesnes, M., Biteau-Coroller, F., Bouyer, J., Dia, M.L., Foil, L., 2009. Development of a mathematical model for mechanical transmission of trypanosomes and other pathogens of cattle transmitted by tabanids. Int. J. Parasitol. 39, 333–346. 2009

Desquesnes, M., Dargantes, A., Lai, D.H., Lun, Z.R., Holzmuller, P., Jittapalapong, S.. Trypanosoma evansi and Surra: a Review and perspectives on transmission, epidemiology and control, impact, and zoonotic aspects. Biomed. Res.Int. http://dx.doi.org/10.1155/2013/321237. 2013

Magnarelli, L.A., Anderson, J.F. Feeding-behavior of Tabanidae (Diptera) on cattle and serological analysis of partial blood meals. Environ. Entomol. 9, 664–667. 1980

Chang, T.T., Chang, T.Y., Chen, C.C., Young, K.C., Roan, J.N., Lee, Y.C., et al. Existence of hepatitis C virus in Culex quinquefasciatus after ingestion of infected blood: experimental approach to evaluating transmission by mosquitoes. J. Clin. Microbiol. 39, 3353–3355. 2001

I find the following comment puzzling: "The iatrogenic transmission that occurred in the 1930s–1950s during a period that coincided with targeted extensive antischistosomal injection campaigns using HCV infected injection equipment could have been avoided by their efforts to clean the injecting equipment if HCV was so easy to neutralise."

This is puzzling because we're talking about a time in history prior to awareness of the stakes. HIV had not been discovered; people (often drug addicts) were paid for blood product donation; and there is good evidence from the Egyptian infection campaign that one practitioner would inject hundreds of people per hour (seconds between injections).

The avoidance of HCV transmission was not a consideration at that time, obviously.

The ongoing epidemic of HCV in Egypt has been overly attributed to the antischistosomal injection campaigns in rural Egypt that ended decades ago. There some serious limitations to the Lancet 2000 report that identified this relationship and there is a serious flaw. The flaw is that the study ignored the concurrent iatrogenic exposures that were even greater throughout the entire country at the time. For those of us that have been working in Egypt as epidemiologists (dating back to the mid 1970s), we are witness to the extraordinary level of iatrogenic exposures at every level of health care delivery both rural and urban. After all, the urban prevalence of HCV antibody is greater than almost anywhere else in the world and schistosomiasis transmission is not urban.

We (my Egyptian colleagues and I) were the first to report this epidemic in Egyptian healthy blood donors and then in a population based community study. We were stunned by how the Lancet 2000 report was used by the health care profession to claim that the epidemic was finished (no more ongoing transmission) since the antischistosomal injection campaigns had ended years before. We and other Egyptian epidemiologists, Talaat et al., have done a great deal to try and overcome this denial but this is not easy. We have been known to refer to this as a Semmelweis effect.  See ref. below

In regard to mother to new borne transmission we have estimated this rate. See ref. below. I appreciate Stuart C Ray’s patience in explaining why HCV is not vector born.   

[1-8]

1.            Benova L, Awad SF, Miller FD, Abu-Raddad LJ. Estimation of hepatitis C virus infections resulting from vertical transmission in Egypt. Hepatology 2015; 61(3): 834-42.

2.            Kamel MA, Ghaffar YA, Wasef MA, Wright M, Clark LC, Miller FD. High HCV prevalence in Egyptian blood donors. Lancet 1992; 340(8816): 427.

3.            Kamel MA, Miller FD, el Masry AG, et al. The epidemiology of Schistosoma mansoni, hepatitis B and hepatitis C infection in Egypt. Ann Trop Med Parasitol 1994; 88(5): 501-9.

4.            Miller F, Abu-Radda L. Evidence of intense ongoing endemic transmission of hepatitis C virus in Egypt. Proc Natl Acad Sci U S A 2010; 107(33): 14757–62.

5.            Mohamoud YA, Mumtaz GR, Riome S, Miller D, Abu-Raddad LJ. The epidemiology of hepatitis C virus in Egypt: a systematic review and data synthesis. BMC Infect Dis 2013; 13: 288.

6.            Talaat M, el-Oun S, Kandeel A, et al. Overview of injection practices in two governorates in Egypt. Trop Med Int Health 2003; 8(3): 234-41.

7.            Talaat M, Kandeel A, Rasslan O, et al. Evolution of infection control in Egypt: achievements and challenges. Am J Infect Control 2006; 34(4): 193-200.

8.            Cuadros DF, Branscum AJ, Miller FD, Abu-Raddad LJ. Spatial epidemiology of hepatitis C virus infection in Egypt: analyses and implications. Hepatology 2014; 60(4): 1150-9.

This discussion about bilharziasis is in fact covering only this historical cause which is not true.  Currently, the main cause of hepatitis C epidemics is iatrogenic due to lack of any sort of quality control on sterilization of surgical interventions. Interventions that are mostly responsible include endoscopies (traditionally all endoscopes are not autoclaved as surgeons are reluctant to risk the lense life, instead they use homemade dilutions of chlorine or other disinfectants for unknown periods of time, totally random), dental procedures, obstetrics and gynecology procedures, and any other surgery in addition to blood banks. In Egypt, the unsupervised private practice represent the major sector that provides actual healthcare. Lack of supervision on that particular point of sterilization of equipment and lack of infection control guidelines is the major cause. Following that, around 10-20% of hepatitis C (globally) is due to unknown causes , suspecting the role of household transmission, which holds true in Egypt, and can be transmitted through hairdresser and other non medical practitioners who have body fluid contaminated equipment poorly sterilized. One more cause among healthcare providers, surgeons are not trained on safe practices during suturing or handing over equipments for example.

I agree completely the No of patients treated /year was about 100000& the newelt infected cases were about 150000 due to lack of infection control in all invasive procedures (e.g Cardiac catheterization. orthopedic surgery ). Nearly all obstetrician not request HBsAg from all pregnant females although it is simple test &cheap but there was no any orientation about this among gynecologists

&obstetricians.

The concept of mechanical transmission, as opposed to biological transmission, in an environment of endemic infection, where there are many more individuals infected and a much higher frequency of insect bites is worth considering. There is significant evidence that HCV survives on the proboscis of arthropods.

Equatorial regions of the world that have endemic infections of mosquito-borne diseases significantly overlap with diseases, such as, malaria, West Nile disease with areas endemic with HCV.

It is recognised that countries with low levels of infection and in moderate climates where insects that transmit infections are rare, transmission though biting insects is so unlikely to be almost impossible. A recent paper, published in the Journal of Medical Virology, presents evidence for the possibility of arthropod transmission in counties like Egypt. Probability of transmission can increase as to the immediate circumstances and conditions at the time. Several factors may enhance mechanical transmission, including high levels of microbes in the vector, frequent biting, the close proximity and contact between vectors and recipients as well as high density of insects. HCV has been isolated from bodies or heads of mosquitoes collected from the houses of HCV-infected individuals.

The possible existence of enzootic cycles of HCV tangential transmission via bridging vectors, such as, arthropods needs to be further investigated and possible animal reservoirs, including domestic rural epizootic cycles for HCV infection, requires much further research with particular initial emphasis on equine infections and the paper hopes to draw attention to this.

I would be astonished if anyone would provide funding to support the investigation of a hypothesis that there is hcv transmission in insects. 

In Egypt the transmission of HCV is iatrogenic. The idea of household transmission or transmission outside the Health Care system was an attempt by the Healthcare System professionals to deflect attention on their own failure to establish infection control. That said there have been improvements in infection control. The need for a truly multi-sectoral effort has yet to be fully realized and attention now is to treat all Egyptians in the country who are infected.

Although there may well still be a significant iatrogenic aspect to this issue, I am aware that some clinicians, especially surgeons, in Egypt are very keen to eradicate this by there own practice and some place the blame on dentists for reusing instruments without the appropriate sterilisation. Obviously improved education in this area is required with healthcare professionals of all such professions. However, there is still considerable evidence of a zoonotic cycle, in addition to this, which has been collated and explored in the attached review journal publication in the Journal of Medical Virology. 

Article Exploring the possibility of arthropod transmission of HCV: ...

if you please, for researchers claiming that the parenteral antischistosomal utilization to be the major cause of high Hep c prevalence in Egypt? what is the primary souce of the virus (formerly known as Non-A non-B virus )?

Mohammad Aziz: There is a non-zero background prevalence of HCV in every country, for reasons that are not yet clear (HCV may have been dispersed in Africa and south Asia millennia ago). The high prevalence of HCV in Egypt (arising from the background low-level infection, hence the dominance of regional subtypes like 4a, 1g, etc) is clearly linked to parenteral exposures, and unsafe injections seem the most strongly supported. The studies cited previously in this thread provide support for the anti-schistosomal injection campaign as a major contributor, but other unsafe injection practices certainly contributed.

Hwer the last demographic survey indicate that the prevalence is decreased to 6%

A new paper shows that HCV can replicate in mosquitos