. Author manuscript; available in PMC: 2015 Jul 1.

Published in final edited form as: J Acquir Immune Defic Syndr. 2014 Jul 1;66(3):316–323. doi: 10.1097/QAI.0000000000000157

Table 4.

The associations of genital tract HIV RNA levels with the natural history (i.e., prevalent and incident detection and persistence) of “any HPV” and “any oncogenic HPV”.

	Prevalence
	Any HPV^a	p-trend	Oncogenic HPV^a	p-trend
Model 1^b	1.57 (1.17–2.11)	0.005^c	2.03 (1.23–3.36)	0.01

Model 1 + CD4 count	1.17 (0.85–1.60)	0.41	1.36 (0.83–2.23)	0.28

Model 1 + CD4 count + plasma HIV viral load	1.20 (0.88–1.62)	0.36	1.36 (0.82–2.25)	0.29

	Incident Detection
	Any HPV^a	p-trend	Oncogenic HPV^a	p-trend

Model 1^b	2.52 (1.70–3.74)	<0.001^c	1.99 (1.15–3.43)	0.02

Model 1 + CD4 count	1.74 (1.15–2.65)	0.01^c	1.51 (0.80–2.88)	0.23

Model 1 + CD4 count + plasma HIV viral load	1.82 (1.12–2.98)	0.02^c	1.79 (0.73–4.39)	0.22

	Persistence
	Any HPV^a	p-trend	Oncogenic HPV^a	p-trend

Model 1^b	1.19 (0.71–2.00)	0.41	2.49 (0.93–6.68)	0.07

Model 1 + CD4 count	1.04 (0.60–1.82)	0.78	2.84 (1.03–7.83)	0.04

Model 1 + CD4 count + plasma HIV viral load	1.14 (0.63–2.08)	0.58	2.66 (0.88–8.07)	0.11

Odds ratio contrasting those women with genital tract HIV RNA levels above the median (545 copies/mL) found in subjects who had detectable values versus those women with undetectable levels

Model 1: a multivariable model adjusted for age, race, smoking, lifetime number of male sex partners, number of male sex partners in the past six months, condom use in the past six months, and cervical treatment in the past six months, and use of highly active anti-retroviral therapy (HAART).