HbC has been described as being more advantageous than HbS because, even in homozygous individuals, it is usually non-fatal. However, in contrast to HbS, it does not prevent malaria due to P. vivax, and is less effective in resistance to falciparum malaria in heterozygous conditions. Homozygous HbC is more resistant to heterozygous condition, or to thalassemias. But HbC mutation  does not prevent the infection. P. falciparum do not survive in red blood cells with homozygous hemoglobins, but can survive in the presence of heterozygous hemoglobins. HbC reduced the binding force (cytoadherence) of P. falciparum by reducing the activity of PfEMP1. Evidences indicate that HbC reduced the level of  PfEMP1, which is required for effective binding and invasion of RBC by the malarial parasite. It has been predicted that with the trend of HbC mutation and falciparum prevalence, HbC would replace HbS in central West Africa in the future. Diagnosis
Physical examination may show an enlarged spleen. Tests that may be done include: complete blood count (CBC), hemoglobin electrophoresis, and peripheral blood smear. Prevention
Genetic counseling may be appropriate for high-risk couples who wish to have a baby. Treatment
Usually no treatment is needed. Folic acid supplementation may help produce normal red blood cells and improve the symptoms of anemia

Prognosis
Overall, hemoglobin C disease is one of the more benign hemoglobinopathies. Mild-to-moderate reduction in RBC lifespan may accompany from mild hemolytic anemia. Individuals with hemoglobin C disease have sporadic episodes of musculoskeletal (joint) pain. People with hemoglobin C disease can expect to lead a normal life.
As a result of this structure-based drug design approach using the Argonne APS, Abbott was able to develop new products that inhibit the protease, and therefore stop virus replication.Lopinavir was developed by Abbott in an attempt to improve upon the companys earlier protease inhibitor, ritonavir, specifically with regard to its serum protein-binding properties (reducing the interference by serum on protease enzyme inhibition) and its HIV resistance profile (reducing the ability of virus to evolve resistance to the drug). Administered alone, lopinavir has insufficient bioavailability; however, like several HIV protease inhibitors, its blood levels are greatly increased by low doses of ritonavir, a potent inhibitor of intestinal and hepatic cytochrome P450 3A4, which would otherwise reduce drug levels through catabolism. Abbott, therefore, pursued a strategy of co-administering lopinavir with doses of ritonavir sub-therapeutic with respect to HIV inhibition; hence, lopinavir was only formulated and marketed as a fixed-dose combination medication with ritonavir.Lopinavir/ritonavir was approved by the US Food and Drug Administration (FDA) on 15 September 2000, and in Europe on 19 March 2001. Its patent was scheduled to expire in the US on 26 June 2016.In March 2020, during the COVID-19 pandemic, the Israeli government announced that it would force AbbVie to license its patents for lopinavir/ritonavir. In response, AbbVie announced that it would cease enforcing its patents on the drug entirely.