HSV-2 Vaccine: Current Status and Insight into Factors  for Developing an Efficient Vaccine

Zhu, Xiaopeng; Muhammad, Zaka S.; Wang, Jianguang; Lin, Wu; Guo, Shikun; Zhang, Wei

doi:10.3390/v6020371

Cited by 37 publications

(41 citation statements)

References 110 publications

(129 reference statements)

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“…Among various means of improving vaccine efficacy, the adoption of adjuvants to promote Ag immunogenicity is one of the simple, yet most effective, ways (5,12). CCL19 was shown to potentiate both cellular and humoral responses to immunogens in mice (16,49), representing a promising molecular adjuvant.…”

Section: Discussionmentioning

confidence: 99%

“…HSV-2 infection can also increase the risk for HIV-1 acquisition by $3-fold (3,4). Despite intensive studies over the last two decades, an effective vaccine against HSV-2 has yet to be developed (5,6).…”

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confidence: 99%

“…HSV-2 glycoprotein B (gB) and glycoprotein D (gD) are the two commonly used immunogens in the development of HSV-2 subunit vaccines (5,(7)(8)(9). However, most findings suggested that one glycoprotein or several glycoproteins in combination are still not sufficient to induce effective immune responses against HSV-2 infection.…”

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confidence: 99%

“…However, most findings suggested that one glycoprotein or several glycoproteins in combination are still not sufficient to induce effective immune responses against HSV-2 infection. One major limitation to subunit protein vaccines or plasmid (p)DNA vaccines encoding such proteins is their poor immunogenicity compared with live-attenuated and inactivated viral vaccines (5,10,11). Adjuvantation is one of the simplest, but most effective, ways to improve the immunogenicity of vaccine candidates (5,12).…”

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confidence: 99%

“…One major limitation to subunit protein vaccines or plasmid (p)DNA vaccines encoding such proteins is their poor immunogenicity compared with live-attenuated and inactivated viral vaccines (5,10,11). Adjuvantation is one of the simplest, but most effective, ways to improve the immunogenicity of vaccine candidates (5,12). Components from the host immune system, such as cytokines, chemokines, and other costimulatory self-molecules, have received much attention as novel molecular adjuvants because of their essential roles in immunocyte differentiation, proliferation, expansion, maturation, and migration (13,14).…”

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confidence: 99%

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Immunization with HSV-2 gB-CCL19 Fusion Constructs Protects Mice against Lethal Vaginal Challenge

Yan

Deng

et al. 2015

The Journal of Immunology

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There is a lack of an HSV-2 vaccine, in part as the result of various factors that limit robust and long-term memory immune responses at the mucosal portals of viral entry. We previously demonstrated that chemokine CCL19 augmented mucosal and systemic immune responses to HIV-1 envelope glycoprotein. Whether such enhanced immunity can protect animals against virus infection remains to be addressed. We hypothesized that using CCL19 in a fusion form to direct an immunogen to responsive immunocytes might have an advantage over CCL19 being used in combination with an immunogen. We designed two fusion constructs, plasmid (p)gBIZCCL19 and pCCL19IZgB, by fusing CCL19 to the C- or N-terminal end of the extracellular HSV-2 glycoprotein B (gB) with a linker containing two (Gly4Ser)2 repeats and a GCN4-based isoleucine zipper motif for self-oligomerization. Following immunization in mice, pgBIZCCL19 and pCCL19IZgB induced strong gB-specific IgG and IgA in sera and vaginal fluids. The enhanced systemic and mucosal Abs showed increased neutralizing activity against HSV-2 in vitro. Measurement of gB-specific cytokines demonstrated that gB-CCL19 fusion constructs induced balanced Th1 and Th2 cellular immune responses. Moreover, mice vaccinated with fusion constructs were well protected from intravaginal lethal challenge with HSV-2. Compared with pgB and pCCL19 coimmunization, fusion constructs increased mucosal surface IgA+ cells, as well as CCL19-responsive immunocytes in spleen and mesenteric lymph nodes. Our findings indicate that enhanced humoral and cellular immune responses can be achieved by immunization with an immunogen fused to a chemokine, providing information for the design of vaccines against mucosal infection by HSV-2 and other sexually transmitted viruses.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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Immunization with HSV-2 gB-CCL19 Fusion Constructs Protects Mice against Lethal Vaginal Challenge

Yan

Deng

et al. 2015

The Journal of Immunology

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Immunopathology of herpes simplex virus‐associated neuroinflammation: Unveiling the mysteries

Hussain,

Gupta,

Samuel

et al. 2023

Reviews in Medical Virology

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The immunopathology of herpes simplex virus (HSV)‐associated neuroinflammation is a captivating and intricate field of study within the scientific community. HSV, renowned for its latent infection capability, gives rise to a spectrum of neurological expressions, ranging from mild symptoms to severe encephalitis. The enigmatic interplay between the virus and the host's immune responses profoundly shapes the outcome of these infections. This review delves into the multifaceted immune reactions triggered by HSV within neural tissues, intricately encompassing the interplay between innate and adaptive immunity. Furthermore, this analysis delves into the delicate equilibrium between immune defence and the potential for immunopathology‐induced neural damage. It meticulously dissects the roles of diverse immune cells, cytokines, and chemokines, unravelling the intricacies of neuroinflammation modulation and its subsequent effects. By exploring HSV's immune manipulation and exploitation mechanisms, this review endeavours to unveil the enigmas surrounding the immunopathology of HSV‐associated neuroinflammation. This comprehensive understanding enhances our grasp of viral pathogenesis and holds promise for pioneering therapeutic strategies designed to mitigate the neurological ramifications of HSV infections.

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Herpes genitalis

Mylonas

2015

Gynäkologe

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Die Infektion mit dem Herpes-simplexVirus (HSV) ist weltweit eine der am häu-figsten auftretenden Viruserkrankungen [18,40,51]. Die Hauptursache des Genitalherpes ist Herpes-simplex-Virus Typ 2 (HSV-2), wobei mittlerweile auch das HSV-1 vermehrt beobachtet wird [5,51]. Obwohl ca. 50-80 % der genitalen Ulzera durch HSV verursacht werden [30,35], sind ca. 75-90 % der infizierten Personen sich dieser Infektion nicht bewusst [13,48].Diese sexuell übertragene Erkrankung verursacht bei den Betroffenen ausgeprägte und schmerzhafte genitale Ulzerationen, den Herpes genitalis. Entscheidend ist dabei, dass das Virus reaktiviert werden kann und es dadurch zu erneuten klinischen Rezidiven kommt. Neben der klinischen Erkrankung kann das Virus auch während der Schwangerschaft auf den Feten bzw. dem Neugeborenen mit teils schweren klinischen Komplikationen und Spätfolgen übertragen werden [14,32,48]. EpidemiologieDie HSV-Seroprävalenz variiert sehr stark aufgrund von Alter, Geschlecht, Ethnizität, Bildungsstand, sozioökono-mischem Status, Region oder sexuellem Risikoprofil [38, 13, 39]. Die Viruspräva-lenz von HSV-2 in der Normalbevölke-rung in einer älteren Untersuchung lag bei 0,25-5 %, während diese bei Frauen mit anderen genitalen Infektionen (z. B. sexuell übertragene Erkrankungen) auf ca. 7 % geschätzt wurde [13]. Mittlerweile zeigt sich in den USA eine Seroprävalenz von ca. 58 % für HSV-1 und 16 % für HSV-2 [38, 51]. Wenngleich HSV-2 die Hauptursache eines genitalen Herpes ist, kommen mittlerweile auch vermehrt genitale Infektionen mit HSV-1 vor [5]. Die Rate einerprimären HSV-1-Infektion ist mittlerweile doppelt so hoch wie von HSV-2 und manifestiert sich häufiger im genitalen als im orofaszialen Bereich [5]. » Die Rate einer primären HSV-1-Infektion ist mittlerweile doppelt so hoch wie von HSV-2 Obwohl die HSV-2-Seroprävalenz zwischen 1970 und 1990 in den USA zunahm [13], zeigte sich ein Rückgang Anfang der 2000er-Jahre (von 21 % in den Jahren 1988 bis 1994 auf 17 % in den Jahren 1999 bis 2004) [51]. Im Gegensatz dazu wurde in den letzten JahrTab. 1 Symptome der Herpes-genitalis-Infektion [33, 34] Mukokutane Manifestation Herpes labialis, Herpes facialis, Herpes integumentalis (vorwiegend durch HSV-1 verursacht) Heilung nach 10 bis 20 Tagen Häufigste Form eines Herpes recurrens oder recidivans Gingivostomatitis und Stomatitis herpetica (primär HSV-1) Herpes genitalis (Vulvovaginitis, Balanitis) Häufigste genital übertragene Kontaktinfektion Tritt nach Primärinfektion und als rekurrierender Herpes auf ZNS-Infektionen Herpes-Enzephalitis ist in Mitteleuropa die häufigste nekrotisierende Enzephalitis (ca. 50 %) 30 % nach Primärinfektionen Bis zu 70 % als rekurrierender Herpes Hohe Letalität (bis zu 70 %), wobei viele überlebende Patienten Residuen behalten Disseminierte Infektionen Disseminierter Herpes simplex mit Streuung des Virus Eczema herpeticatum Beteiligung des Auges (primär HSV-1) Ösophagitis Hepatitis Beteiligung von weiteren inneren Organen (HSV-1 und HSV-2) mit oft tödlichem Verlauf zehnten eine ansteigende In...

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HSV-2 Vaccine: Current Status and Insight into Factors for Developing an Efficient Vaccine

Cited by 37 publications

References 110 publications

Immunization with HSV-2 gB-CCL19 Fusion Constructs Protects Mice against Lethal Vaginal Challenge

Immunization with HSV-2 gB-CCL19 Fusion Constructs Protects Mice against Lethal Vaginal Challenge

Immunopathology of herpes simplex virus‐associated neuroinflammation: Unveiling the mysteries

Herpes genitalis

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