Events that lead to viral infections include the binding of the virus to the target cells, internalization of the virus into the cells, and the ability of the viral genome to be expressed. These steps are mediated by cellular and viral proteins and are temporally regulated. The papillomavirus capsid consists of two virally encoded capsid proteins, L1 and L2. Much is known about the role of the major capsid protein L1 compared to what is known of the role of the L2 protein. We identified the interaction of the L2 protein with SNARE protein syntaxin 18, which mediates the trafficking of vesicles and their cargo between the endoplasmic reticulum, the cis-Golgi compartment, and possibly the plasma membrane. Mutations of L2 residues 41 to 44 prevented the interaction of L2 protein with syntaxin 18 in cotransfection experiments and resulted in noninfectious pseudovirions. In this paper, we describe that syntaxin 18 colocalizes with infectious bovine papillomavirus type 1 (BPV1) pseudovirions during infection but does not colocalize with the noninfectious BPV1 pseudovirions made with an L2 mutant at residues 41 to 44. We show that an antibody against BPV1 L2 residues 36 to 49 (␣L2 36-49) binds to in vitro-generated BPV1 pseudoviral capsids and does not coimmunoprecipitate syntaxin 18-and BPV1 L2-transfected proteins. ␣L2 36-49 was able to partially or completely neutralize infection of BPV1 pseudovirions and genuine virions. These results support the dependence of syntaxin 18 during BPV1 infection and the ability to interfere with infection by targeting the L2-syntaxin 18 interaction and further define the infectious route of BPV1 mediated by the L2 protein.Papillomaviruses (PVs) induce a variety of lesions such as cutaneous or genital warts in humans and exophytic papillomas of cutaneous or mucosal epithelia in animals. Human PV (HPV) infection is the most common sexually transmitted disease in the United States (approximately 5.5 million cases per annum) (31), and specific HPV genotypes (high risk) are the etiologic agents of cervical carcinoma, a major killer of women worldwide (23,(37)(38)(39). Bovine PV (BPV) infection causes benign tumors, which can result in squamous cell carcinoma in the presence of environmental factors such as bracken (7).The PV capsids consist primarily of two virally encoded proteins, L1 and L2, at an estimated ratio of 30:1 (17, 49). The L1/L2 ratio suggests that there is one L2 at each of 12 capsid vertices (49). Each viral particle contains a single doublestranded circular DNA genome of about 8 kb bound by histone proteins (15, 24), and the virus is assembled in the nucleus of squamous epithelial cells into particles that are 52 to 55 nm in diameter (9).The expression of the viral L1 protein in the absence of other viral proteins results in the packaging of viral DNA at inefficient levels (5, 50). The addition of L2 to viral particle production increases DNA packaging into virions (28, 53) and contributes to the infectious process of the virus (2, 18). Antibodies to L2 have proven to be ...
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