TY  - JOUR
AB  - Human endogenous retroviruses (HERVs), which are normally silenced by methylation or mutation, can be reactivated by a variety of environmental factors, including infection with exogenous viruses. In this work, we investigated the transcriptional activity of HERVs following infection of human liver cells (HepaRG) with human adenovirus C serotype 5 (HAdV-C5). HAdV-C5 infection results in reactivation of several HERV groups as well as differentially expressed genes. Interestingly, in HAdV-C5 infection, upregulated genes that were in close chromosomal proximity to upregulated HERV loci were associated with influencing viral carcinogenesis and inflammatory signaling. We also identified an FBXO17 transcript encoding an intronic ERVK9-11 sense sequence upon HAdV-C5 infection. FBXO17 has previously been described as an important factor in the regulation of the interferon response. This suggests that specific HERV groups may have the potential to trigger gene networks and influence viral immune responses.
AU  - Liang, W.
AU  - Stubbe, M.*
AU  - Pleninger, L.
AU  - Hofferek, A.*
AU  - Stubbe, H.C.*
AU  - Mai, J.*
AU  - Özer, S.
AU  - Frishman, D.*
AU  - Schreiner, S.
AU  - Vincendeau, M.
C1  - 72889
C2  - 56775
CY  - Radarweg 29, 1043 Nx Amsterdam, Netherlands
TI  - HERV reactivation by adenovirus infection is associated with viral immune regulation.
JO  - Microbes Infect.
VL  - 27
IS  - 5-6
PB  - Elsevier
PY  - 2024
SN  - 1286-4579
ER  - 

TY  - JOUR
AB  - Human norovirus (HuNoV) is a major global cause of acute gastroenteritis, with vaccine development facing several challenges. Despite years of research, there are currently no licensed vaccines available for controlling HuNoVs. Here, we describe the construction and testing of a replication-deficient Sendai virus (SeV) vector as a potential vaccine candidate against the HuNoV GII.4 genotype. SeV was chosen as the vaccine backbone due to its non-pathogenic nature in humans, its capability for long-term antigen expression in mammalian cells, and its suitability for mucosal administration. By inserting the HuNoV GII.4 capsid gene, VP1, into the SeV genome, we generated a replication-deficient SeV (SeV/dP.VP1) vector. The resultant SeV/dP.VP1 virus were observed to successfully express the inserted NoV VP1 gene upon infection. Inoculating the vaccine into wild-type mice elicited NoV-specific IgG antibodies, along with INF-γ and IL-2-producing T cells, through both intranasal (i.n.) and intramuscular (i.m.) immunization. Furthermore, a significant level of NoV-specific IgA was detected in lung homogenates after i.n. immunization, particularly using a high dose of the viral vector. Additionally, a synergistic effect was observed with heterologous prime-boost regimens using SeV/dP.VP1 and MVA.VP1 vectors, indicating the potential for more robust immune responses when the vaccine design is optimized. Our study demonstrates the potential of a SeV vaccine candidate in eliciting a broad immune response and lays the foundation for further exploration of the SeV vector platform's potential as a HuNoV vaccine. Additionally, the results emphasize the importance of vaccine dosage and administration route, highlighting the need for tailored immunization strategies.
AU  - Samieipour, Y.*
AU  - Wiegand, M.
AU  - Willner, E.M.*
AU  - Hoffmann, D.*
AU  - Shameli, K.*
AU  - Protzer, U.
AU  - Moeini, H.*
C1  - 71639
C2  - 56328
TI  - Replication-deficient sendai virus expressing human norovirus capsid protein elicits robust NoV-specific antibody and T-cell responses in mice.
JO  - Microbes Infect.
PY  - 2024
SN  - 1286-4579
ER  - 

TY  - JOUR
AB  - The potential of an attenuated Salmonella enterica serovar Typhimurium strain as a prophylactic anti-tumor vaccine against the murine fibrosarcoma WEHI 164 was evaluated. Tumor cells were transfected with the DNA sequence encoding the MHC class I-restricted peptide p60(217-225) from Listeria monocytogenes. BALB/c mice received a single orogastric immunization with Salmonella that translocates a chimeric p60 protein via its type III secretion system. Mice were subsequently challenged subcutaneously with p60(217-225)-expressing WEHI cells. In vivo protection studies revealed that 80% of these mice remained free of the fibrosarcoma after challenge, whereas all animals of the non-vaccinated control group did develop tumor growth. In further experiments, the distribution of tetramer-positive p60(217-225)-specific effector and memory CD8 T cells after Salmonella-based immunization and tumor application was analyzed. Costaining with CD62L and CD127 revealed a predominance of p60-specific central memory and effector memory CD8 T cells in spleens, whereas in blood samples the majority of p60-specific lymphocytes belonged to effector and effector memory CD8 T cell subsets. This is the first report demonstrating that a bacterial type III secretion system can be used for heterologous antigen delivery to induce cytotoxic effector and memory CD8 T cell responses resulting in an efficient prevention of tumor growth.
AU  - Panthel, K.*
AU  - Meinel, K.M.*
AU  - Domenech, V.E.S.*
AU  - Geginat, G.*
AU  - Linkemann, K.*
AU  - Busch, D.H.
AU  - Rüssmann, H.*
C1  - 1716
C2  - 24023
SP  - 2539-2546
TI  - Prophylactic anti-tumor immuntiy against a murine fibrosarcoma triggered by the Salmonella type III secretion system.
JO  - Microbes Infect.
VL  - 8
IS  - 9-10
PB  - Elsevier
PY  - 2006
SN  - 1286-4579
ER  - 

TY  - JOUR
AB  - Modified vaccinia virus Ankara (MVA) is a potent vaccine vector, which proved its safety, immunogenity and efficacy in preclinical and clinical studies. The rational for the development of a vaccine against HIV based on the regulatory protein Nef delivered by MVA combined with a V2-deleted Env protein is discussed.
AU  - Erfle, V.
AU  - Göbel, F.D.*
AU  - Guzman, C. A.*
AU  - Le Grand, R.*
C1  - 4498
C2  - 23325
SP  - 1400-1404
TI  - Vaccines based on Nef and on Nef/(Delta)V2 Env.
JO  - Microbes Infect.
VL  - 7
PY  - 2005
SN  - 1286-4579
ER  - 

TY  - JOUR
AU  - Wilhelm, P.
AU  - Wiede, F.*
AU  - Meissner, A.*
AU  - Donhauser, N.*
AU  - Bogdan, C.*
AU  - Körner, H.*
C1  - 5402
C2  - 23543
SP  - 1461-1468
TI  - TNF but not Fas ligand provides protective anti-L. major immunity in C57BL/6 mice.
JO  - Microbes Infect.
VL  - 7
PY  - 2005
SN  - 1286-4579
ER  -