China
Africa
Explore chapters and articles related to this topic
Order Martellivirales: Togaviridae
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
Garg et al. (2020) generated a universal VLP vaccine termed CJaYZ targeting not only CHIKV but also Japanese encephalitis (JEV), yellow fever (YFV), and Zika (ZIKV) viruses from the Flaviviridae family, order Amarillovirales (see Chapter 22). For CHIKV, the vaccine included C-E3-E2-E1 genes. The stable 293T cell lines secreting VLPs containing capsid protein for all four viruses were established and adapted to grow in suspension cultures to facilitate vaccine scale up. The immunization of mice with different combinations of the capsid protein containing VLPs either as monovalent, bivalent, or tetravalent formulation resulted in generation of high levels of neutralizing antibodies. The potential tetravalent VLP vaccine candidate provided strong neutralizing antibody titers against all four viruses (Garg et al. 2020).
Zika: An Ancient Virus Incipient into New Spaces
Published in Jagriti Narang, Manika Khanuja, Small Bite, Big Threat, 2020
Bennet Angel, Neelam Yadav, Jagriti Narang, Surender Singh Yadav, Annette Angel, Vinod Joshi
Zika virus is an insect-borne virus (arbovirus), belonging to the Flavivirus genus in the Flaviviridae family, which causes fever. It is somewhat similar to dengue, yellow fever, West Nile fever, Japanese encephalitis, and viruses that are members of the family Flaviviridae. It is an enveloped, icosahedral, non-segmented, single-stranded, positive-sense RNA genetic material. The diameter of viral entities is 40 nm composed of external envelop and interior dense core. The size of ZIKV genome is 10,617 nucleotides that synthesize three configural proteins such as capsid, membrane, and envelope-154 glycosylation motif, which is responsible for causing virulency. Besides these structural proteins, viral genome also synthesizes several nonstructural proteins such as NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5 (Fig. 6.3) (Modis et al., 2003; Rey et al., 1995; Zhang, W. et al., 2003; Zhang, Y. et al., 2003, 2004).
Yellow Fever
Published in Rae-Ellen W. Kavey, Allison B. Kavey, Viral Pandemics, 2020
Rae-Ellen W. Kavey, Allison B. Kavey
The family Flaviviridae contains three genera: the above-described flaviviruses, which include yellow fever virus (YFV), West Nile virus (WNV), dengue virus (DENV) and Zika virus (ZIKV); the hepaci-viruses, which include hepatitis B and C viruses; and the pesti-viruses, which infect hoofed mammals. The vector-borne arboviruses are grouped as a clade within the Flavivirus genus and this is subdivided into a mosquito-borne clade and a tick-borne clade. The mosquito clade is divided into two branches: one branch contains the neurotropic viruses, often associated with encephalitic disease in humans or livestock. This branch tends to be spread by the Culex mosquito species and to have bird reservoirs – an example is the West Nile virus. The second branch is the group associated with hemorrhagic disease in humans. These tend to have Aedes species as vectors and primate hosts – the yellow fever virus is emblematic of this group.46
The next generation of HCV vaccines: a focus on novel adjuvant development
Published in Expert Review of Vaccines, 2021
Kimia Kardani, Seyed Mehdi Sadat, Mona Kardani, Azam Bolhassani
In the 1970s, most blood transfusion infections were linked to either hepatitis A or B virus. Primarily known as ‘non-A, non-B’ hepatitis, HCV was first recognized after discovery of its genome in 1989 [17]. The virus is a member of the Hepacivirus genus and Flaviviridae family that possesses an envelope and positive-sense single stranded ribonucleic acid (RNA) genome (9.6 kb). Figure 1 illustrates the structure of HCV. The genome of HCV is translated into a single large polyprotein containing approximately 3,000 amino acids, which is processed into 10 mature viral proteins by viral and cellular proteases. These viral proteins are divided into three structural proteins (core, E1, E2) and seven non-structural (NS) proteins (p7, NS2, NS3, NS4A, NS4B, NS5A, NS5B) [2]. The genome organization of HCV is shown in Figure 2. There are eight major HCV genotypes [18], and genotype 1 is the most prevalent, followed by genotypes 3, 4 and 2. There is about 30% genetic diversity among various HCV genotypes [18,19]. Moreover, HCV is called lipo-viro particles due to a fusion between cellular and viral components. Cellular proteins involved in the lipo-viro particles are apolipoproteins (Apo) A-I, Apo B, APO c-II, and Apo E [20–22].
An update on dengue vaccine development, challenges, and future perspectives
Published in Expert Opinion on Drug Discovery, 2021
Fakhriedzwan Idris, Donald Heng Rong Ting, Sylvie Alonso
A number of hypotheses that involve both viral and host factors have been proposed to explain dengue pathogenesis and have been reviewed in detail elsewhere [7,8]. Severe cases have been associated with secondary heterologous infections, and this was proposed to be due to the presence of antibodies produced during the primary DENV infection that bind to but do not neutralize the heterologous DENV, and facilitate entry inside FcγR-expressing permissive cells, leading to increased viral loads and enhanced disease severity, a term coined antibody-dependent enhancement (ADE) [3]. Presence of IgG antibodies specific to Japanese encephalitis virus, another member of the Flaviviridae family, was also proposed to cause ADE upon primary DENV infection [9]. Antibodies produced against prM protein and the fusion loop in E protein have been shown to play a role in ADE [4]. In addition, FcγR-mediated DENV infection was found to suppress effectively the host antiviral innate immunity, thereby further promoting DENV intracellular replication [10]. Furthermore, enhanced disease severity upon secondary heterologous DENV infection has also been attributed to the reactivation of weakly cross-reactive memory T cells generated during the primary DENV infection. These T cells display limited antiviral capacity but secrete high amounts of pro-inflammatory cytokines such as TNF-α that contribute to plasma leakage [11]. This concept known as ‘original antigenic sin’ remains however controversial with conflicting studies and lack of strong evidence in dengue patients.
Post-exposure prophylactic vaccine candidates for the treatment of human Risk Group 4 pathogen infections
Published in Expert Review of Vaccines, 2020
James Logue, Ian Crozier, Peter B Jahrling, Jens H Kuhn
Finally, tick-borne encephalitis virus (TBEV; Flaviviridae: Flavivirus) is generally transmitted by ixodid ticks in Western (Ixodes ricinus) and Eastern (Ixodes persulcatus) Europe. The virus is maintained by over 100 species of wild animals, including voles, deer, and domestic animals such as sheep [122–124]. Although patients infected with TBEV normally only present with an initial, nonspecific febrile phase, 20–30% of patients progress to a second stage of disease with CNS signs (meningitis, encephalitis, or both). Lethality is generally 1–2%, but 30–60% of patients develop chronic neuropsychiatric sequelae [125,126]. Three different vaccines for pre-exposure disease prevention (IPVE, FSME-IMMUN, and Encepur) are generally available in endemic regions [127]. However, fears over the potential of antibody-dependent disease enhancement or increased viral infectivity caused by ‘sub-optimal’ concentrations of virus-specific antibodies have hampered further vaccine development [128]. For this reason and the potential of other adverse effects [129], none of these vaccines are licensed by the US FDA. Vaccine use is neither recommended by the US Centers for Disease Control and Prevention (CDC) nor the WHO except for high-risk individuals, such as laboratory workers or workers with high exposure to potentially infected host ticks [130,131]. Multiple studies into the use of antibody treatments as PEP have produced promising results in laboratory mice with no disease enhancement [132,133].