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8 pages, 3068 KB

Open AccessArticle

Persistent Rhesus Enteric Calicivirus Infection in Recombinant CHO Cells Expressing the Coxsackie and Adenovirus Receptor

by Tibor Farkas and Zeinab R. Aboezz

Viruses 2024, 16(12), 1849; https://doi.org/10.3390/v16121849 - 28 Nov 2024

Cited by 2 | Viewed by 1511

Abstract

Recently, using a panel of recombinant CHO cell lines, we identified the coxsackie and adenovirus receptor (CAR) and histo-blood group antigens (HBGAs) or sialic acid as the minimum requirement for susceptibility to rhesus enteric calicivirus (ReCV) infections. While ReCVs cause lytic infection in LLC-MK2 cells, recombinant CHO (rCHO) cell lines did not exhibit any morphological changes upon infection. To monitor infectious virus production, rCHO cell cultures had to be freeze–thawed and titrated on LLC-MK2 monolayers. This raised the question of whether ReCV infection in rCHO cells is persistent and whether non-enveloped progeny virions are released from the infected cells. Here, we used the rCHO-CAR+ cell line and a CAR and sialic acid-dependent recovirus strain (FT7) and found that these cells were persistently infected, and infectious virus was continuously produced and released into the culture without showing any visible cell damage. Viral capsid protein and replication intermediate double-stranded RNA (dsRNA) were detectable in almost all cells for at least 12 passages. We suspect a fully exosomal viral exit mechanism without a lytic cycle in these cells. rCHO cell may provide a valuable system for ReCV production (producer cell line) and serve as a model for investigating enteric calicivirus non-lytic viral exit mechanisms and the properties of the released, most likely membrane-cloaked, infectious progeny virions. Full article

(This article belongs to the Section Animal Viruses)

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20 pages, 1766 KB

Open AccessReview

Hepatitis E Virus: What More Do We Need to Know?

by Endrit Shahini, Antonella Argentiero, Alessandro Andriano, Francesco Losito, Marcello Maida, Antonio Facciorusso, Raffaele Cozzolongo and Erica Villa

Medicina 2024, 60(6), 998; https://doi.org/10.3390/medicina60060998 - 18 Jun 2024

Cited by 7 | Viewed by 10394

Abstract

Hepatitis E virus (HEV) infection is typically a self-limiting, acute illness that spreads through the gastrointestinal tract but replicates in the liver. However, chronic infections are possible in immunocompromised individuals. The HEV virion has two shapes: exosome-like membrane-associated quasi-enveloped virions (eHEV) found in circulating blood or in the supernatant of infected cell cultures and non-enveloped virions (“naked”) found in infected hosts’ feces and bile to mediate inter-host transmission. Although HEV is mainly spread via enteric routes, it is unclear how it penetrates the gut wall to reach the portal bloodstream. Both virion types are infectious, but they infect cells in different ways. To develop personalized treatment/prevention strategies and reduce HEV impact on public health, it is necessary to decipher the entry mechanism for both virion types using robust cell culture and animal models. The contemporary knowledge of the cell entry mechanism for these two HEV virions as possible therapeutic target candidates is summarized in this narrative review. Full article

(This article belongs to the Special Issue Viral Hepatitis Research: Updates and Challenges)

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14 pages, 2312 KB

Open AccessArticle

Nonenveloped Avian Reoviruses Released with Small Extracellular Vesicles Are Highly Infectious

by Zuopei Wang, Menghan He, Han He, Kyle Kilby, Roberto de Antueno, Elizabeth Castle, Nichole McMullen, Zhuoyu Qian, Tzviya Zeev-Ben-Mordehai, Roy Duncan and Chungen Pan

Viruses 2023, 15(7), 1610; https://doi.org/10.3390/v15071610 - 23 Jul 2023

Cited by 11 | Viewed by 2910

Abstract

Vesicle-encapsulated nonenveloped viruses are a recently recognized alternate form of nonenveloped viruses that can avoid immune detection and potentially increase systemic transmission. Avian orthoreoviruses (ARVs) are the leading cause of various disease conditions among birds and poultry. However, whether ARVs use cellular vesicle trafficking routes for egress and cell-to-cell transmission is still poorly understood. We demonstrated that fusogenic ARV-infected quail cells generated small (~100 nm diameter) extracellular vesicles (EVs) that contained electron-dense material when observed by transmission electron microscope. Cryo-EM tomography indicated that these vesicles did not contain ARV virions or core particles, but the EV fractions of OptiPrep gradients did contain a small percent of the ARV virions released from cells. Western blotting of detergent-treated EVs revealed that soluble virus proteins and the fusogenic p10 FAST protein were contained within the EVs. Notably, virus particles mixed with the EVs were up to 50 times more infectious than virions alone. These results suggest that EVs and perhaps fusogenic FAST-EVs could contribute to ARV virulence. Full article

(This article belongs to the Section Animal Viruses)

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18 pages, 3819 KB

Open AccessArticle

The Capsid (ORF2) Protein of Hepatitis E Virus in Feces Is C-Terminally Truncated

by Takashi Nishiyama, Koji Umezawa, Kentaro Yamada, Masaharu Takahashi, Satoshi Kunita, Mulyanto, Isao Kii and Hiroaki Okamoto

Pathogens 2022, 11(1), 24; https://doi.org/10.3390/pathogens11010024 - 26 Dec 2021

Cited by 14 | Viewed by 4073

Abstract

The hepatitis E virus (HEV) is a causative agent of hepatitis E. HEV virions in circulating blood and culture media are quasi-enveloped, while those in feces are nonenveloped. The capsid (ORF2) protein associated with an enveloped HEV virion is reported to comprise the translation product of leucine 14/methionine 16 to 660 (C-terminal end). However, the nature of the ORF2 protein associated with fecal HEV remains unclear. In the present study, we compared the molecular size of the ORF2 protein among fecal HEV, cell-culture-generated HEV (HEVcc), and detergent-treated protease-digested HEVcc. The ORF2 proteins associated with fecal HEV were C-terminally truncated and showed the same size as those of the detergent-treated protease-digested HEVcc virions (60 kDa), in contrast to those of the HEVcc (68 kDa). The structure prediction of the ORF2 protein (in line with previous studies) demonstrated that the C-terminal region (54 amino acids) of an ORF2 protein is in flux, suggesting that proteases target this region. The nonenveloped nondigested HEV structure prediction indicates that the C-terminal region of the ORF2 protein moves to the surface of the virion and is unnecessary for HEV infection. Our findings clarify the maturation of nonenveloped HEV and will be useful for studies on the HEV lifecycle. Full article

(This article belongs to the Special Issue Hepatitis E and the One-Health Aspect: A Threat to Mankind and Animality?)

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10 pages, 738 KB

Open AccessReview

Hepatitis E Virus Entry

by Xin Yin and Zongdi Feng

Viruses 2019, 11(10), 883; https://doi.org/10.3390/v11100883 - 20 Sep 2019

Cited by 41 | Viewed by 10326

Abstract

Hepatitis E virus (HEV) infection is a major cause of acute hepatitis worldwide. It is transmitted enterically but replicates in the liver. Recent studies indicate that HEV exists in two forms: naked, nonenveloped virions that are shed into feces to mediate inter-host transmission, and membrane-cloaked, quasienveloped virions that circulate in the bloodstream to mediate virus spread within a host. Both virion types are infectious, but differ in the way they infect cells. Elucidating the entry mechanism for both virion types is essential to understand HEV biology and pathogenesis, and is relevant to the development of treatments and preventions for HEV. This review summarizes the current understanding of the cell entry mechanism for these two HEV virion types. Full article

(This article belongs to the Special Issue Hepatitis E Virus)

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18 pages, 5080 KB

Open AccessArticle

Cleavage of the HPV16 Minor Capsid Protein L2 during Virion Morphogenesis Ablates the Requirement for Cellular Furin during De Novo Infection

by Linda Cruz, Jennifer Biryukov, Michael J. Conway and Craig Meyers

Viruses 2015, 7(11), 5813-5830; https://doi.org/10.3390/v7112910 - 11 Nov 2015

Cited by 21 | Viewed by 7829

Abstract

Infections by high-risk human papillomaviruses (HPV) are the causative agents for the development of cervical cancer. As with other non-enveloped viruses, HPVs are taken up by the cell through endocytosis following primary attachment to the host cell. Through studies using recombinant pseudovirus particles (PsV), many host cellular proteins have been implicated in the process. The proprotein convertase furin has been demonstrated to cleave the minor capsid protein, L2, post-attachment to host cells and is required for infectious entry by HPV16 PsV. In contrast, using biochemical inhibition by a furin inhibitor and furin-negative cells, we show that tissue-derived HPV16 native virus (NV) initiates infection independent of cellular furin. We show that HPV16 L2 is cleaved during virion morphogenesis in differentiated tissue. In addition, HPV45 is also not dependent on cellular furin, but two other alpha papillomaviruses, HPV18 and HPV31, are dependent on the activity of cellular furin for infection. Full article

(This article belongs to the Section Animal Viruses)

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