The Question of HIV Vaccine: Why Is a Solution Not Yet Available?

Table 1

HIV-1 main genes and protein functions encoded.

Class	Gene	Polyprotein	Protein(s)	Function(s)	References
Viral structural proteins	gag	Gag	Matrix (MA, p17); Capsid (CA, p24); Nucleocapsid (NC, p7)	Encodes a polyprotein that is processed to form the structural proteins placed inside the envelope	[23, 24]
	pol	Pol	Protease (PR, p12); Reverse transcriptase (RT, p66) and RNaseH (p51); Integrase (IN, p32)	Proteolytic cut of Gag/Pol proteins.; When in the cytoplasm, RT transcribes viral RNA into a complementary copy of DNA, resulting in the formation of dsDNA. RNaseH degrades viral RNA.; In the nucleus, the integration of HIV dsDNA occurs into the host cellular genome by IN (formation of the provirus)	[24, 25]
	env	PrGp (gp160)	Surface protein (SU, gp120); Transmembrane protein (TM, gp41)	It fuses the viral and cell membranes after binding to the cellular receptor; gp160 undergoes a series of conformational changes, and it is cleaved in gp120 and gp41	[24, 26]
Essential regulatory elements	tat	—	Tat	Transactivator; activates transcription of viral DNA and cellular genes	[27]
	rev	—	Rev	Gene transcription regulator of virion proteins. Rev facilitates viral unspliced mRNAs transport from the nucleus to the cytoplasm for their translation	[25]
Accessory regulatory proteins	nef	—	Negative regulating factor	Nef is a protein that affects HIV replication, viral particle infectivity, CD4 downregulation and apoptosis	[24]
	vif	—	Viral infectivity factor	Vif regulates virus infectivity through the degradation of human APOBEC3G (cellular cytidine deaminase) protein, which provide innate immunity against various pathogens	[28]
	vpr	—	Viral protein R	Vpr controls the import of the HIV-1 dsDNA preintegration complex into the nucleus, the activation and apoptosis of infected cells, virus transcription, and cell cycle arrest	[29]
	vpu	—	Viral protein U	Vpu increases the release of viral particles from human cells and contributes to the overall downregulation of CD4s expression throughout HIV-1 infection by inducing their degradation	[30]