**Author details**

3TC and efavirenz just under three months after exposure to HIV and within one month of confirmed seroconversion, after an acute viral illness had his viral load below limit of detection

proteins in any tissue/organ compartment after treatment interruption for nine years [121]. This case shows evidence of strong and broad CD8 T-cell responses and strong proliferative CD4 T-cell responses. What might be responsible for this? In contrast, analysis of the CCR5 coreceptor showed that the homozygous CCR5 promoter A59029G was present, but no delta 32 deletion was observed [121] and the HLA-I subtype was A 01, 02 B:44, 52. Nevertheless, HIV was recovered later from the patients using a humanised mouse model after transplan‐ tation of the patient's purified CD4 T-cells and anti-CD3/anti-CD28 stimulation. This indicated the presence of HIV capable of replication and that other factors other than CCR5 mutation may be responsible for viral control. The French VISCONTI cohort study also reported patients who started treatment early and was able to gain control of the virus replication with unde‐ tected viral load after six years of treatment interruption [122]. A period of at least four years

In most studies, preferential attention has been given to latent resting CD4+ T-lymphocytes as a source of HIV persistence in the cell and CCR5 coreceptor mutation as responsible for HIV control. While explanations for functional cure have proved inadequate, ROS has been demonstrated to contribute to disease progression and drug design [124]. New strategies for HIV functional cure should incorporate use of ROS-activated prodrugs [113]. Adequate data on OS condition of spontaneous controllers (natural resistance) and the posttreatment controllers (PTC)/functional cure are not available. Luc Montagner, codiscoverer of the HIV, identified oxidative stress as one of the four factors responsible for its variability [125]. Besides, recent report that P13K/Akt inhibitors can drastically sensitise HIV-infected macrophages (reservoir) to oxidative-stress-induced cell death [126] indicates possible ROS therapeutic approach to achieve HIV cure as well as the cytoprotective effect of the virus-activated P13K/ AKt in human microglial cell line and macrophages against apoptotic challenge [127]. In addition, HIV infection increases the cellular levels of ROS, especially superoxide anion and peroxynitrite which accelerates HIV replication in macrophages [28]. Recently, Bhaskar et al. demonstrated that a marginal increase of about ~25mV in *E*GSH is sufficient to switch HIV-1 from latency to reaction using Grx1-roGFP2 biosensor [128], suggesting possibility of purging HIV-1 by redox modulators which shows how fluctuations in *E*GSH modulate expression of

HIV host reservoir of latently infected cells stands as the barrier to a successful longed-for cure that would free HIV-positive patients from a lifetime of taking antiretroviral drugs. Antire‐ trovirals known to protect uninfected cells reduce the viral load and stave off full-blown AIDS. However, they do not eliminate the HIV reservoir in the host. Though the virus is not com‐ pletely eradicated in EC, the reservoir could not replicate, so low viral load is recorded and antiretrovirals are unnecessary. OS however has been implicated in HIV replication and

). He has shown no HIV RNA or associated

with stable range of CD4 cell (900–1,000 cells/mm3

196 Trends in Basic and Therapeutic Options in HIV Infection - Towards a Functional Cure

of treatment is suggested prior to treatment interruption [123].

antioxidant gene in infected HIV patients [129].

**9. Conclusion**

Ibeh Bartholomew Okechukwu\*

Address all correspondence to: barthokeyibeh@yahoo.com

Medical Biotechnology Department,National Biotechnology Development Agency, Abuja, Nigeria
