How virus persistence can initiate the tumorigenesis process

doi:10.5501/wjv.v2.i2.102

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May 12, 2013 (publication date) through Dec 1, 2024

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World Journal of Virology

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2220-3249

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Virol. May 12, 2013; 2(2): 102-109
Published online May 12, 2013. doi: 10.5501/wjv.v2.i2.102

Table 2 Viral proteins inducing genetic damage

Virus	EBV	HHV-8	HPV	HBV	HCV	HTLV-1
Latent proteins	EBNA-1	LANA-1[64]	E6, E7[66,67]	Naturally occurring pre-S mutants[68]	-	-
	EBNA-3C	v-CYC[65]
	LMP-1[63]
Lytic proteins	BZLF-1[69]	-	E1, E2[71,72]	HBx[73,74]	Core	Tax[76,77]
	BGLF-5[70]				NS3[23,62]
					NS5[75]

EBV: Epstein-Barr virus; HHV-8: Human herpesvirus 8, also named Kaposi sarcoma virus; HPV: Human papillomavirus; HBV: Hepatatis B virus; HCV: Hepatitis C virus; HTLV-1: Human T-cell leukemia virus 1.

Citation: Avanzi S, Alvisi G, Ripalti A. How virus persistence can initiate the tumorigenesis process. World J Virol 2013; 2(2): 102-109
URL: https://www.wjgnet.com/2220-3249/full/v2/i2/102.htm
DOI: https://dx.doi.org/10.5501/wjv.v2.i2.102