Researchers try' to uncover the role of diseases and disease-causing organisms in evolution
EVOLUTION has moulded living creatures
in such a manner that their ability
to survive an reproduce is constantly
improving. on a rough sense, one
may say that given two populations,
one of ancestors and a second of
descendants, the descendants will carry
a subset of ancestral genes: genes which
contribute to a higher fitness are more
likely to persist and spread than those
genes that are relatively less capable of
doing so.
Renowned biologist J B S Haldane
had said more than forty years ago
that the course of evolution has been
moulded to a large extent by disease and
disease-causing organisms. A con-
temporary look at Haldane's thesis
from the specific angle of malaria is the
subject of a recent article by G Pasvol of
the Imperial College School of Medi-
cine, UK (The Lancet, Vol 348, No 903 1).
Because the signature of evolutionary
change is a change in the genetic make-up of organisms, the first thing to ask is, are there genes that look as if they have
evolved in the course of the fight against
malaria? It appears that there may be
two such sets, both recognised by the
diseases they can lead to. One disease is
known as sickle cell anemia and the
other, thalassemia. Both are due to
changes in the sequence of the DNA that
codes for haemoglobin, the protein that
transports oxygen to the tissues. Note
the seeming paradox: the genetic
changes that we are talking about are
both helpful (if they help us counteract
malaria, that is) and harmful (because
they demonstrably also cause disease).
The sickle cell part of the story is reasonably well understood.
There is a variant version, or allele,
of the normal ('A') haemoglobin gene
and it is known as the s allele.
Individuals with two copies of the s
allele suffer from severe anaemia, but
those with one copy of s and one copy of
A are resistant to malaria whereas those
with two copies of A are not. The basis of
the resistance can vary. The s allele can
affect the entry of malarial parasites into
red cells, or the development of parasites within infected cells, or cause the
removal of infected cells from the system, or all three. Therefore, it persists in the population by virtue of its presence.
SS combinations, meaning individuals
suffering from sickle cell anaemia, are
born in every generation. As one might
expect on the basis of this correlation,
the s allele tends to be found in those
parts of the world that have had a history
of malarial infection.
The thalassemia story is not as clear. What is becoming
evident, though, is that thalassemia has affected human
genes in a big way. An intriguing finding that
has emerged recently is that individuals with
alpha thalassemia have higher
risks of clinical malaria (invasion of red cells by
the parasite) than others, a paradoxical finding if the gene is
supposed to offer protection. The suggestion made by Pasvol and
co-workers is that such clinical
infection might act as a live
natural vaccine and hasten the
acquisition of immunity from the disease itself. Unfortunately,
it is not easy to prove this hypothesis because as of today there is no clear-cut laboratory method of demonstrating immunity against malaria.
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