Literature on vulvar cancer (VC) and vulvar intraepithelial neoplasia (VIN) in women living with HIV (WLWH) is scarce with no data on human papillomavirus (HPV) genotyping.We compared disease characteristics and HPV genotyping on biopsies from WLWH and HIV-negative women (HNW) followed for VIN2+ (VIN2/3 and VC) at Saint-Pierre Hospital between 2000 and 2022. Then, a case control study identified VIN2+ risk factors among WLWH with VIN2+ (cases) and WLWH without VIN followed at the same period (controls), matched for age, ethnicity, and HIV follow-up duration.Compared to 65 HNW (28 VC/37 VIN), 25 WLWH (4 VC/21 VIN) were younger at time of VIN2+ diagnosis (48 vs. 58.7 years, p < 0.001), had more frequently cervical or anal (multicentric) dysplasia (52% vs. 22%, p = 0.02) and non-excisional treatments, and less often healthy margins in excisions (14% vs. 43%, p = 0.02). In WLWH, high-risk HPV was found in 100% (vs. 85% in HNW) with more multiple genotype infections (40% vs. 13%); HPV16 was found in 80% of VC and 73% of VIN in WLWH versus 91% and 79% in HNW. Compared to 75 controls, 25 cases had significantly more frequently prior cervical high-grade intraepithelial lesion (HSIL) (40%), lower median CD4-lymphocyte count (382/μL), and shorter duration of undetectable HIV viremia (4.8 years) than controls (respectively 0%, p = 0.001; 770 CD4/μL, p = 0.021; 10.6 years, p = 0.04).WLWH develop VIN2+ younger than HNW, with more multiple HPV infections but less HPV 16, more multicentric lesions, and less excisions with negative margins. Risk factors for developing VIN2+ in WLWH include lack of viremia control and immunosuppression.