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- The Role of Extracellular Vesicles in Pandemic Viral Infections.
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Woosung Shim, Anjae Lee, Jung-Hyun Lee
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J. Microbiol. 2024;62(6):419-427. Published online June 25, 2024
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DOI: https://doi.org/10.1007/s12275-024-00144-x
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Abstract
- Extracellular vesicles (EVs), of diverse origin and content, are membranous structures secreted by a broad range of cell types. Recent advances in molecular biology have highlighted the pivotal role of EVs in mediating intercellular communication, facilitated by their ability to transport a diverse range of biomolecules, including proteins, lipids, DNA, RNA and metabolites. A striking feature of EVs is their ability to exert dual effects during viral infections, involving both proviral and antiviral effects. This review explores the dual roles of EVs, particularly in the context of pandemic viruses such as HIV-1 and SARS-CoV-2. On the one hand, EVs can enhance viral replication and exacerbate pathogenesis by transferring viral components to susceptible cells. On the other hand, they have intrinsic antiviral properties, including activation of immune responses and direct inhibition of viral infection. By exploring these contrasting functions, our review emphasizes the complexity of EV-mediated interactions in viral pathogenesis and highlights their potential as targets for therapeutic intervention. The insights obtained from investigating EVs in the context of HIV-1 and SARS-CoV-2 provide a deeper understanding of viral mechanisms and pathologies, and offer a new perspective on managing and mitigating the impact of these global health challenges.
- Manganese Transporter Proteins in Salmonella enterica serovar Typhimurium
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Nakyeong Ha , Eun-Jin Lee
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J. Microbiol. 2023;61(3):289-296. Published online March 2, 2023
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DOI: https://doi.org/10.1007/s12275-023-00027-7
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Abstract
- The metal cofactors are essential for the function of many enzymes. The host restricts the metal acquisition of pathogens for
their immunity and the pathogens have evolved many ways to obtain metal ions for their survival and growth. Salmonella
enterica serovar Typhimurium also needs several metal cofactors for its survival, and manganese has been found to contribute
to Salmonella pathogenesis. Manganese helps Salmonella withstand oxidative and nitrosative stresses. In addition,
manganese affects glycolysis and the reductive TCA, which leads to the inhibition of energetic and biosynthetic metabolism.
Therefore, manganese homeostasis is crucial for full virulence of Salmonella. Here, we summarize the current information
about three importers and two exporters of manganese that have been identified in Salmonella. MntH, SitABCD, and ZupT
have been shown to participate in manganese uptake. mntH and sitABCD are upregulated by low manganese concentration,
oxidative stress, and host NRAMP1 level. mntH also contains a Mn2+-
dependent riboswitch in its 5′ UTR. Regulation of
zupT expression requires further investigation. MntP and YiiP have been identified as manganese efflux proteins. mntP is
transcr!ptionally activated by MntR at high manganese levels and repressed its activity by MntS at low manganese levels.
Regulation of yiiP requires further analysis, but it has been shown that yiiP expression is not dependent on MntS. Besides
these five transporters, there might be additional transporters that need to be identified.
- Protective and pathogenic role of humoral responses in COVID-19
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Uni Park , Nam-Hyuk Cho
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J. Microbiol. 2022;60(3):268-275. Published online March 2, 2022
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DOI: https://doi.org/10.1007/s12275-022-2037-8
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Abstract
- Since the advent of SARS-CoV-2 in Dec. 2019, the global endeavor
to identify the pathogenic mechanism of COVID-19
has been ongoing. Although humoral immunity including
neutralizing activity play an important role in protection from
the viral pathogen, dysregulated antibody responses may be
associated with the pathogenic progression of COVID-19,
especially in high-risk individuals. In addition, SARS-CoV-2
spike-specific antibodies acquired by prior infection or vaccination
act as immune pressure, driving continuous population
turnover by selecting for antibody-escaping mutations.
Here, we review accumulating knowledge on the potential
role of humoral immune responses in COVID-19, primarily
focusing on their beneficial and pathogenic properties. Understanding
the multifaceted regulatory mechanisms of humoral
responses during SARS-CoV-2 infection can help us to develop
more effective therapeutics, as well as protective measures
against the ongoing pandemic.
- Transmissibility and pathogenicity of SARS-CoV-2 variants in animal models
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Young-Il Kim , Mark Anthony B. Casel , Young Ki Choi
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J. Microbiol. 2022;60(3):255-267. Published online March 2, 2022
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DOI: https://doi.org/10.1007/s12275-022-2033-z
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8
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Abstract
- As of February 2022, SARS-CoV-2 is still one of the most
serious public health threats due to its high mortality rate and
rapid spread of novel variants. Since the first outbreak in 2019,
general understanding of SARS-CoV-2 has been improved
through basic and clinical studies; however, knowledge gaps
still exist in our understanding of the emerging novel SARSCoV-
2 variants, which impacts the corresponding development
of vaccines and therapeutics. Especially, accumulation of
mutations in SARS-CoV-2 and rapid spread in populations
with previous immunity has resulted in selection of variants
that evade the host immune response. This phenomenon threatens
to render current SARS-CoV-2 vaccines ineffective for
controlling the pandemic. Proper animal models are essential
for detailed investigations into the viral etiology, transmission
and pathogenesis mechanisms, as well as evaluation of the
efficacy of vaccine candidates against recent SARS-CoV-2
variants. Further, the choice of animal model for each research
topic is important for researchers to gain better knowledge
of recent SARS-CoV-2 variants. Here, we review the advantages
and limitations of each animal model, including mice,
hamsters, ferrets, and non-human primates, to elucidate variant
SARS-CoV-2 etiology and transmission and to evaluate
therapeutic and vaccine efficacy.
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