## 4 Discussion  
With the inception of highly active antiretroviral therapy (HAART), the quality of life of HIV-infected patients has seen a major transition and has increased life expectancy. The combination of drugs efficiently suppresses an HIV viral load, thereby prolonging the life of HIV/AIDS patients almost to one of the general population. However, HIV infection leads to pronounced oxidative stress through various mechanisms by which the virus triggers ROS production [34]. Virus triggered ROS production is a strong modulator of the immune system leading to opportunistic infections [34]. Thus, such effects need to be controlled and targeted for immune suppression of viral replication. In a wide range of disease states characterized by increased oxidative stress, antioxidants have been demonstrated to boost immune function as reported in human intervention studies [35]. Furthermore, immune modulators, which are potential candidates in the prevention and treatment of HIV/AIDS, are thoroughly reviewed and reported elsewhere [36]. Research findings have demonstrated that an alteration of the intracellular redox balance characterizes several viral infections and the progression of viral-induced diseases [5]. In case of HIV, it has been suggested that increased levels of inflammatory cytokines can induce both depletion of GSH and oxidative stress [34; 37; 38; 39]. GSH, being the most powerful antioxidant, puts the cell at risk for oxidant damage when it is deficient. It has been observed that a wide range of pathologies, including cancer, and many viral infections, including HIV-1, leads to an imbalance in GSH levels, and various reports have provided evidence for the use of GSH molecules being able to replenish intracellular GSH levels during antiviral therapy [2; 11; 34]. While the combined use of antioxidants and chemotherapeutic agents has been explored, the interactive effects of using ARVs and AOs are very limited. The drug of interest in the present investigation was efavirenz (EFA), which remains the ARV of choice when it comes to the treatment of individuals co-infected with mycobacterial infections. Efavirenz is known to exhibit similar behaviour to so-called brick dust drugs due to its high melting point and stable crystalline structure in which strong intermolecular bonds significantly limit the dissolution and bioavailability of their pharmaceutical forms [40]. Poor solubilization of efavirenz, a benzoxazinone compound with 40 to 45% of oral bioavailability, obscures its therapeutic functionality. To enhance the therapy of HIV infection, lipid-based oral drug delivery systems of such poorly soluble drugs are under investigation. Nevertheless, various other lipid carriers of EFA are reported by several authors [41; 42; 43; 44; 45]. However, liposomal delivery to achieve effective drug concentrations in viral reservoirs has gained importance in the last few decades, yet EFA delivery by way of liposomes is limited. Furthermore, its co-delivery along with GSH is not reported so far. Another molecule, nevirapine belonging to the group of NNRTI, has been reported to be loaded into liposomal formulations to improve targeted delivery to select compartments in the cells, thereby alleviating systemic toxic side effects [46]. By application of film hydration procedure, liposomes incorporating EFA with and without GSH were prepared to obtain encapsulation efficiency up to the range of 90%. The encapsulation efficiency of GSH was less prominent, which could mean that a substantial amount of GSH was present in the aqueous core. Furthermore, the polydispersity index less than 0.3 indicated a narrow size distribution and homogenous distribution of colloidal particles, hence a good quality for all the formulations. Furthermore, a large negative zeta potential further enhanced the stability of vesicular suspension by simple electrostatic stabilisation with negativity being imparted by phospholipid and cholesterol.