In the past genotype 2 and 3 information has been
lumped together. More recent information has emerged that there are
clear differences between these 2 genotypes with respect to prevalence,
disease progression and treatment cure rates. Interestingly, there is
also substantial data about how genotype 2 migrated from Africa to
other parts of the world via the slave trade in the 16th,17th, and 18th centuries.
There are 7 HCV genotypes identified numbered 1 through 7. The most common genotypes worldwide include:
Genotype 1 (46.2%)
Genotype 3 (30.1%)
Genotype 2 (9.1%)
Genotype 4 (8.3%)
Genotype 6 (5.4%)
Genotype 5 (.8%)
So far, there has only been 1
person identified with genotype 7. Thirteen to 15% of people with
hepatitis C in the United States are infected with genotype 2.
As noted above, 9.1% of the
population worldwide has gentoype 1. This translates to about 16.5
million people infected with HCV genotype 2 globally. Areas that have a
prevalence of 10% or greater include:
Central Latin America— 19.3%
High-income Asia Pacific—24.5%
High-income North America—12.0%
West Sub-Saharan Africa—23.0%
The most common genotype 2 subtypes include 2a, 2b, 2c, but there have been 15 other subtypes identified.
Technology is amazing! Science can analyze the
genetic make-up of hepatitis C virus to estimate the origin, date it
and track the viral migration. Previous studies were able to deduce
that genotype 2 originated in West Africa at least 500 years ago.
In the current study
“Phytogeography and molecular epidemiology of hepatitis C virus
genotype 2 in Africa,” by P.V. Markov et al., the authors wanted to
understand where genotype 2 originated. The study group looked at all
the known subtypes of genotype 2, then concentrated on the geographical
area of Guinea-Gambia, which had been theorized as the origin of
genotype 2. Using a process called the molecular clock the authors
confirmed that Guinea-Gambia was indeed the source of genotype 2.
Genotype 2 then spread from West Africa to Central Africa.
Blood-to-blood contact transmits
hepatitis C. This being the case, it is likely that the spread of
hepatitis C through Africa occurred over hundreds of years. So what
made hepatitis C increase in such large numbers and spread throughout
all of West Africa and Central Africa faster? It is most likely that
hepatitis C was spread throughout Africa by European campaigns to treat
endemic diseases in Africa with injectable medications.
Trypanosomiasis (sleeping sickness), syphilis, yaws, malaria, and
leprosy were (and some still are) rampant in Africa. Treating these and
other diseases was well-intentioned but, unfortunately, the needles
were reused or not properly cleaned. Millions of unsafe injections
were given in Africa before the advent of disposal needles, which
contributed to the spread of hepatitis C in Africa.
With regard to how genotype 2
was spread beyond Africa that question has also been answered based on
the same genetic technology. The introduction of genotype 2 into
America—particularly in Central and South America—was the result of the
transatlantic slave trade from West Africa. This is called viral
This is the same way that yellow
fever (in the same viral family as the hepatitis C virus—flavivirus
family) and other diseases common in Africa were introduced into the
Americas by the same transatlantic slave trade. Similarly, European
diseases such as smallpox, measles, tuberculosis, and influenza were
introduced into the Americas by the Europeans.
Genotype 2 is also common in
Europe not only because of the slave trade, but also due to
immigration. France is believed to have contributed to the migration of
genotype 2 from their West African colonies to other colonies in
Morocco, Quebec, and Vietnam (French Indochina). It appears that
genotype 2i in France was introduced by West African conscripts trained
and stationed in southern France during World War I—but this needs to
be confirmed by larger studies.
Genotype 2 did not only migrate
from Africa to the Americas and Europe, it also migrated from South
America to Asia. This occurred by way of the slave trade from Java,
Indonesia to Surinam (South America) and then back to Indonesia in the
Genotype 2 does not increase the risk for HCV
disease progression. This is in stark contrast to genotype 3, which
has been found to increase the risk for steatosis (fatty liver) and HCV
disease progression, including higher rates of fibrosis and steatosis.
The American Association for the Study of Liver
Diseases (AASLD) and the Infectious Disease Society of American (IDSA)
recommend that genotype 2 should be treated with the combination of
Sovaldi (sofosbuvir a pill taken once-a-day) plus ribavirin (a pill
taken twice daily—dosage based on a person’s body weight). The
duration of treatment with Sovaldi is 12 weeks.
The cure rates are:
AASLD/IDSA also recommend that
previous non-responders to therapy can include peginterferon in the 12
weeks of therapy. Patients who were previous non-responders with
cirrhosis may benefit by extending treatment duration to 16 weeks.
There is such a high cure rate
for genotype 2 that there is very little research looking at new
therapies to treat HCV genotype 2. However, due to the high cost of
current treatments, newer inexpensive therapies would be a welcome
addition to the treatment landscape of genotype 2, especially in