It is a common misconception that thals are immune to malaria. Thalassemia does offer some protection against malaria but thals do indeed contract malaria. Usually what this means is that the malaria will not be as serious compared to a non thal's malaria. However, if the immune system is already low due to other factors, a patient will more easily succumb. I know Hamza had various health issues over the years, and these may have been contributing factors, along with the throat infection.
For more on malaria, read this previous thread at
http://www.thalassemiapatientsandfriends.com/index.php?topic=474.0I'd like to clear up a mis-conception about thals and malaria. Thals can and do get malaria. However, malaria does not usually thrive in the blood of thals, resulting in much milder cases that lead to improved immunities against malaria. In fact, it has been found that thals who have had a case of the less severe type of malaria, develop some immune protection against the more serious strain of malaria. There are two types of malaria virus. P. Vivax is the milder form. Studies showed that young alpha thals were more susceptible to p. vivax but that infection led to a higher resistance to the more deadly P. Falciparum later in life. It seems the only benefit is resistance to malaria and the researchers suggested that the rate of the thal gene would be even higher in the malaria regions if not for the negative effects of thal. Considering the devastating effects of malaria, the protection given by the thal gene is very significant.
Recent research suggests that the higher fetal hemoglobin levels often found in thals have much to do with why the malaria virus does not thrive in thals.
From
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=9746793&dopt=AbstractPlusWe conclude that HbF provides protection from P falciparum malaria by the retardation of parasite growth. The mechanism involves resistance to digestion by malarial hemoglobinases based on the data presented and with the well-known properties of HbF as a super stable tetramer. In addition, the resistance of normal neonates for malaria can now be explained by a double mechanism: increased malaria invasion rates, reported in neonatal RBC, will direct parasites to fetal cells, as well as F cells, and less to the approximately 20% of HbA containing RBC, amplifying the antimalarial effects of HbF.
We have learned that some thals produce much more HbF than other thals and this may also provide some explanation as to why not all thals react the same way to a malaria infection.