The serologic response against virus-like particles (VLP) from 7 high risk genital papillomaviruses was investigated by ELISA in 147 Colombian women with invasive cervical cancer and 147 age-matched cytologically normal and HPV-DNA negative women. Anti-VLP antibodies were detected in 82% of the invasive cervical cancer patients and in 56% of the controls. Detection of antibodies against multiple HPV types is the rule and the presence of high antibody titers was associated with higher survival of cancer patients. Higher anti-VLP seroprevalence was observed in younger cancer patients. In those followed serologically for 1 year, antibodies generally remained at the same level. However, in some patients an increase or decrease in antibody levels occurred simultaneously for multiple HPV types, suggesting cross-reactivity between the HPV types investigated. Investigation of seroreactivity between 8 high risk HPVs suggested that there is some cross-reactivity between phylogeneticaly-related types such as 16, 31, 33 and 58; and 18, 45 and 59. In conclusion, our results confirmed (i) the high rate of HPV infections in Colombia, both in patients with cervical cancer and in the general population, and the particularly high rate of infections due to HPV 31 and 58; and (ii) the validity of anti-VLPs as a marker of present or past HPV infection. The simultaneous appearance or disappearance of antibodies against multiple HPV VLPs suggests that the antibodies detected by ELISA are not always type specific. © 2002 Wiley-Liss, Inc. Key words: HPV; virus-like particles; cervical cancer; anti-VLP antibodiesCancer of the uterine cervix is one of the most common malignancies in women world wide. 1,2 and the contribution of high risk or oncogenic genital human papillomaviruses (HPVs) in the development of such cancers is well established. [3][4][5][6] Cohort studies indicate that HPV infection with oncogenic types is mostly transient and that only a small proportion of those infected become carriers and then develop cervical intraepithelial neoplasia. [7][8][9][10][11][12] Over 100 HPV genotypes have been identified, 6,13 of which approximately 40 types infect the anogenital tract. The etiologic role of papillomavirus in cervical cancer has been recognized for only a limited number of them, including in decreasing order. 14 The geographical distribution of oncogenic HPV types in cervical cancers shows that HPV-16 is the most common type in all regions, followed by HPV-18. However, there are some geographical differences. For example HPV-33, -39, -58 and -59 are more common in Latin America than in other regions. 4,12,15 Colombia has one of the highest incidences of cervical cancer in the world (48 cases/ 100,000 women/year 1 ) and the most common types detected in Colombia are HPV-16, followed by HPV 58. 16,17 Numerous serologic studies using mainly HPV-16 VLPs 18 -27 have demonstrated that infection with genital HPVs is followed by a serologic immune response to viral capsid proteins and that anti-VLP antibodies can be an indicat...
The major structural protein (VP1) of the BK polyomavirus (BKV) was expressed in the recombinant baculovirus expression system. Recombinant BKV VP1 was shown to self-assemble into virus-like particles (VLPs) with a diameter of 45-50 nm. As for other polyomaviruses, BKV VP1 has the capacity to bind to exogenous DNA. Furthermore, the potential of BKV VP1 VLPs was investigated for gene transfer into COS-7 cells using three methods for the formation of pseudo-virions : disassembly/reassembly, osmotic shock and direct interaction between VLPs and reporter plasmid DNA. The latter method was shown to be the most efficient when using linearized plasmid. Gene transfer efficiency with BKV pseudo-virions was of the same order as that observed with human papillomavirus type 16 L1 protein VLPs. In addition, it is demonstrated that cellular entry of BKV pseudo-virions is dependent on cell surface sialic acid.Human BK polyomavirus (BKV) is a member of the family Polyomaviridae, genus Polyomavirus, a family which also includes simian virus 40 (SV40), JC virus (JCV) and other animal polyomaviruses such as murine polyomavirus. Primary infection with BKV and JCV leads to lifetime persistence in the kidney, CNS and in lymphoid cells (Do$ rries, 1998). BKV\ human cohabitation is considered to be an innocent relationship and most infections, which occur early in childhood, are asymptomatic. BKV is regarded as an opportunistic pathogen in immunocompromised patients and is frequently recovered from the urine of kidney and bone marrow transplant recipients. In such patients, BKV infection has been associated
Artificial viruses consisting of DNA plasmid packaged in vitro into virus-like particles (VLPs) are new vehicles for gene transfer. We therefore investigated the ability of nine human papillomavirus (HPV) VLPs to interact with heterologous DNA and transfer genes. HPV 16,18, 31, 33, 39, 45, 58, 59, and 68 VLPs were able to bind heterologous DNA and to transfer genes into Cos-7 cells. Inhibition of gene transfer by preincubation of the pseudovirions with heparin confirmed that heparan sulfate on the cell surface plays a role as cell receptor for HPVs. As HPV neutralizing antibodies are mainly type-specific, gene transfer with different HPV pseudovirions offers the possibility of their sequential use in vivo for a greater efficacy. ß
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