The Ins and Outs of Multipartite Plant Viruses

Ins and Outs of Multipartite Plant Viruses Viruses possessing a non-segmented genome require a specific recognition of their nucleic acid to ensure its protection in a capsid. A similar feature exists for viruses having a segmented genome, usually consisting of viral genomic segments joined together into one viral entity. While this appears as a rule for animal viruses, the majority of segmented plant viruses package their genomic segments individually. To ensure a productive infection, all viral particles and thereby all segments have to be present in the same cell. Progression of the virus within the plant requires as well a concerted genome preservation to avoid loss of function. This review discusses the replication of chosen phytoviruses and argue for the existence of RNA-RNA interactions that drive the preservation of viral genome integrity while the virus progresses in the plant.


Ins and Outs of Multipartite Positive-Strand RNA Plant Viruses: Packaging versus Systemic Spread. Viruses 2016, 8(8), 228; doi: 10.3390/v8080228

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The Buzz about Honey Bee Viruses

The Buzz about Honey Bee Viruses This short review presents current understanding of the role of viruses on honey bee health and address some overarching questions in honey bee virology.

  • Why Should I Be Concerned about Honey Bee Colony Losses and What Is Colony Collapse Disorder (CCD)?
  • What Are the Most Common Viruses Infecting Honey Bees and How Do They Impact Bee Health?
  • How Are Bee Viruses Transmitted?
  • What Are the Mechanisms of Honey Bee Antiviral Defense?
  • What Is the Future of Honey Bee Virology?


The Buzz about Honey Bee Viruses. (2016) PLoS Pathog 12 (8): e1005757. doi: 10.1371/journal.ppat.1005757

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Assessing the global threat from Zika virus

Mosquito-carried diseases First discovered in 1947, Zika virus (ZIKV) infection remained a little-known tropical disease until 2015, when its apparent association with a considerable increase in the incidence of microcephaly in Brazil raised alarms worldwide. There is limited information on the key factors that determine the extent of the global threat from ZIKV infection and resulting complications. This review describes what is known about the epidemiology, natural history, and public health effects of ZIKV infection, the empirical basis for this knowledge, and the critical knowledge gaps that need to be filled.

“The evidence highlighted in this review is both encouraging and disheartening. On the one hand, the speed with which the global community has collected and disseminated clinical, epidemiologic, and laboratory information on ZIKV after identification of the threat is impressive. But the development of therapeutics and diagnostics is hampered by our ignorance, despite knowing of ZIKV’s existence for more than half a century. Consequently, we have been able to do little to contain the virus’s rapid spread across the Americas. New threats from infectious diseases may emerge from unexpected places, and we need strategies in place that we can roll out to rapidly gain an understanding of the transmission, pathogenesis, and control of previously little-known pathogens to protect global public health.”


Assessing the global threat from Zika virus. (2016) Science 353(6300): aaf8160. doi: 10.1126/science.aaf8160

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Where are things inside a bacterial cell?

Bacteria Bacterial cells are intricately organized, despite the lack of membrane-bounded organelles. The extremely crowded cytoplasm promotes macromolecular self-assembly and formation of distinct subcellular structures, which perform specialized functions. For example, the cell poles act as hubs for signal transduction complexes, thus providing a platform for the coordination of optimal cellular responses to environmental cues. Distribution of macromolecules is mostly mediated via specialized transport machineries, including the MreB cytoskeleton. Recent evidence shows that RNAs also specifically localize within bacterial cells, raising the possibility that gene expression is spatially organized. This review describes the current understanding of where things are in bacterial cells and discuss emerging questions that need to be addressed in the future.

  • Bacterial cells are intricately organized, with many proteins and RNAs being specifically localized.
  • The poles of rod-shaped bacterial cells are emerging as subcellular regions of importance for sensing and signaling.
  • The MreB cytoskeletal system plays an important role in cellular trafficking of macromolecules.
  • Subcellular domains in bacterial cells are connected through a complex network of interactions.


Where are things inside a bacterial cell? (2016) Current Opinion in Microbiology 33: 83–90. doi: 10.1016/j.mib.2016.07.003

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Common Human Mutations That Protect against Infectious Disease

DNA For millennia, pathogens and human hosts have engaged in a perpetual struggle for supremacy. From the earliest recorded smallpox epidemics around 1350 B.C.E to the Black Death due to Yersinia pestis in the Middle Ages and continuing to modern times with HIV, there has been a continuous clash between pathogens and human hosts. But past pandemics are more than just ancient history—they are drivers of human genetic diversity and natural selection. Pathogens can dramatically decrease survival and reproductive potential, leading to selection for resistance alleles and elimination of susceptibility alleles. Despite this persistent struggle between host and pathogen, only in the past century have we developed an understanding of some of the human genetic differences that regulate infectious disease susceptibility and severity.

Studies identifying and characterizing alleles associated with infectious diseases from around the world have led to a better understanding of how the history of past pandemics is written in our genomes. The selective force of infectious diseases has had lasting impacts on our genetic susceptibility to ancient and emerging infections as well as autoimmune and chronic diseases. This story is ongoing and changes will continue to be written into our genomes by new and future infectious diseases.

The Legacy of Past Pandemics: Common Human Mutations That Protect against Infectious Disease. (2016) PLoS Pathog 12(7): e1005680. doi: 10.1371/journal.ppat.1005680

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How many bacteria?

Tree of Life I’ve asked the question How many different bacterial species are there on this blog before. It seems that we may be approaching an answer.

A census of species of Archaea and Bacteria published recently showed that, despite ever-increasing sequencing efforts, the PCR-based retrieval of 16S rRNA genes is approaching saturation. On average, 95% of the genes analyzed today are identical to those present in public databases, with rarefaction analysis indicating that about one-third of the bacterial and archaeal diversity has already been covered. Despite previous estimates of up to 1012 microbial species, the option should be considered that the census of Archaea and Bacteria on planet Earth might yield only millions of species after all.

After All, Only Millions? MBio. 2016 Jul 5; 7(4). pii: e00999-16. doi: 10.1128/mBio.00999-16

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Emerging Paramyxoviruses – Receptor Tropism and Zoonotic Potential

MERS-CoV Emerging infectious disease events are dominated by zoonoses: infections that are naturally transmissible from animals to humans or vice versa. A worldwide survey of ~5,000 bat specimens identified 66 novel paramyxovirus species – more than double the existing total within this family of viruses. Also, novel paramyxoviruses are continuously being discovered in other species, such as rodents, shrews, wild and captivated reptiles and farmed fish, as well as in domestic cats and horses. Paramyxoviruses exhibit one of the highest rates of cross-species transmission among RNA viruses, and paramyxoviral infection in humans can cause a wide variety of often deadly diseases. Thus, it is important to understand the determinants of cross-species transmission and the risk that such events pose to human health. Whilst pathogen diversity and human encroachment play important roles, This paper focuses on receptor tropism and envelope determinants for zoonosis of emerging paramyxoviruses.


Emerging Paramyxoviruses: Receptor Tropism and Zoonotic Potential. (2016) PLoS Pathog 12(2): e1005390. doi: 10.1371/journal.ppat.1005390

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HTLV-1 Replication: An Update

HTLV-1 Replication I spent more than 10 years working on HTLV, the first human retrovirus to be discovered, but it was a long time ago (propably before most of the people reading this now were born :-)
It’s good to get an update on recent research in this field, although as the authors of this article point out:

“As the first human retrovirus discovered in the early 1980s, HTLV-1 has been studied extensively, yet there is still no treatment or vaccine for HTLV-1 infection.”

Molecular Studies of HTLV-1 Replication: An Update. (2016) Viruses 8(2), 31; doi: 10.3390/v8020031
Human T-cell leukemia virus type 1 (HTLV-1) was the first human retrovirus discovered. Studies on HTLV-1 have been instrumental for our understanding of the molecular pathology of virus-induced cancers. HTLV-1 is the etiological agent of an adult T-cell leukemia (ATL) and can lead to a variety of neurological pathologies, including HTLV-1-associated-myelopathy/tropical spastic paraparesis (HAM/TSP). The ability to treat the aggressive ATL subtypes remains inadequate. HTLV-1 replicates by (1) an infectious cycle involving virus budding and infection of new permissive target cells and (2) mitotic division of cells harboring an integrated provirus. Virus replication initiates host antiviral immunity and the checkpoint control of cell proliferation, but HTLV-1 has evolved elegant strategies to counteract these host defense mechanisms to allow for virus persistence. The study of the molecular biology of HTLV-1 replication has provided crucial information for understanding HTLV-1 replication as well as aspects of viral replication that are shared between HTLV-1 and human immunodeficiency virus type 1 (HIV-1). Here in this review, we discuss the various stages of the virus replication cycle—both foundational knowledge as well as current updates of ongoing research that is important for understanding HTLV-1 molecular pathogenesis as well as in developing novel therapeutic strategies.

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Towards a cure for herpesvirus infection with CRISPR/Cas9

Bovine herpesvirus Most adults carry multiple herpesviruses. Following the initial acute infection, these viruses establish life-long infections in their hosts and cause cold sores, keratitis, genital herpes, shingles, infectious mononucleosis, and other diseases. Some herpesviruses can cause cancer in man. During the latent phase of infection, the viruses remain dormant for long periods of time, but retain the capacity to cause occasional reactivations, that may lead to disease. This new study suggests that attacking herpesvirus DNA with CRISPR/Cas9 genome editing technology can suppress virus replication and, in some cases, lead to elimination of the virus from infected cells.

The snag? Well this is a purely in vitro study in cultured cell, not even an animal model. Will this approach be safe and effecting in humans? It will take some years to find that out.


CRISPR/Cas9-Mediated Genome Editing of Herpesviruses Limits Productive and Latent Infections. (2016) PLoS Pathog 12(6): e1005701. doi: 10.1371/journal.ppat.1005701

Herpesviruses infect the majority of the human population and can cause significant morbidity and mortality. Herpes simplex virus (HSV) type 1 causes cold sores and herpes simplex keratitis, whereas HSV-2 is responsible for genital herpes. Human cytomegalovirus (HCMV) is the most common viral cause of congenital defects and is responsible for serious disease in immuno-compromised individuals. Epstein-Barr virus (EBV) is associated with infectious mononucleosis and a broad range of malignancies, including Burkitt’s lymphoma, nasopharyngeal carcinoma, Hodgkin’s disease, and post-transplant lymphomas. Herpesviruses persist in their host for life by establishing a latent infection that is interrupted by periodic reactivation events during which replication occurs. Current antiviral drug treatments target the clinical manifestations of this productive stage, but they are ineffective at eliminating these viruses from the infected host. Here, we set out to combat both productive and latent herpesvirus infections by exploiting the CRISPR/Cas9 system to target viral genetic elements important for virus fitness. We show effective abrogation of HCMV and HSV-1 replication by targeting gRNAs to essential viral genes. Simultaneous targeting of HSV-1 with multiple gRNAs completely abolished the production of infectious particles from human cells. Using the same approach, EBV can be almost completely cleared from latently infected EBV-transformed human tumor cells. Our studies indicate that the CRISPR/Cas9 system can be effectively targeted to herpesvirus genomes as a potent prophylactic and therapeutic anti-viral strategy that may be used to impair viral replication and clear latent virus infection.

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