Table 3.

—Summary of the Proposed Mechanisms Linking HIV With Lung Cancer

Theory	Mechanisms	Key References
Direct oncogenic effect of HIV	Virus-inducing microsatellite alterations and widespread genomic instability.	Wistuba et al43
	Tat, an essential gene for HIV-1 replication, increases expression of protooncogenes and proliferation of the human adenocarcinoma cell line by downregulating tumor suppressor gene p53.	el-Solh et al44
	Downregulation of HIV Tat-interacting protein (TIP30) has been found to promote metastasis of lung cancer.	Baker et al,45 Tong et al46
HIV-induced immunosuppression	Conflicting evidence, wherein immunosuppression may lead to a reduction in tumor surveillance, thus enabling tumor growth.	Bower et al,15 Engels47
Chronic inflammation	Chronic inflammation has been recognized as a risk factor for lung cancer.	Engels48
	Individuals with HIV infection and chronic pneumonia and asthma are at higher risk of lung cancer.	Shebl et al,49 Kirk et al41
	The rate of pneumonia is nearly six times higher in patients with HIV infection and CD4 counts > 500 cells/μL than in control subjects without HIV.	Sogaard et al50
Cigarette smoking	Smoking is an independent risk factor for lung cancer in individuals with HIV infection.	Guiguet et al28
	Smoking is two to three times more prevalent among individuals with HIV infection than in the general population.	Engels et al,18 Giordano and Kramer51
IV drug use	IV drug users with HIV infection have an increased risk of lung cancer compared with nonusers with HIV.	Serraino et al52

Tat = transactivator of transcription.