Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:List the steps of replication and explain what occurs at each stepDescribe the lytic and lysogenic cycles of virus replicationExplain the transmission and diseases of animal and plant virusesDiscuss the economic impact of animal and plant viruses

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Chronic hepatitis B virus (HBV) infection can damage the liver, resulting in a type of scarring called fibrosis. Fibrosis can lead to cirrhosis, liver cancer, and death, so it’s important to understand exactly how HBV causes it. One important event in fibrosis is the activation of liver cells called hepatic stellate cells (HSCs). HBV can activate HSCs directly by interacting with or possibly infecting them to alter gene and protein expression. It can also activate HSCs indirectly by infecting other liver cells and causing them to release inflammatory molecules like TGF-β and CTGF. These mediators can then bind to receptors on HSCs and trigger numerous signaling pathways. The inflammatory molecules also recruit immune cells such as monocytes, macrophages, T cells, and natural killer cells to the liver. These cells perpetuate the inflammatory state and can secrete more HSC-activating molecules like interleukins..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Rabies causes severe neurological symptoms and has a high mortality rate, killing over 59,000 people each year. Rabies virus encodes five phosphoproteins (P) that are involved in viral genomic replication, transport, oxidative stress, interferon antagonism, and autophagy induction. Unfortunately, the specific functions of each P protein are poorly understood. A recent study zeroed in on the viral protein P5. Using cell lines, researchers found that P5 attaches to the N-terminal residues of the protein beclin1 (BECN1). P5 binding to the ring-like structure of BECN1 induced incomplete autophagy due to incomplete fusion with lysosomes. This process promoted rabies virus replication by increasing the levels of viral proteins. Silencing the gene for beclin1 did not reproduce this pattern of P5-induced viral replication. This study identifies for novel role for P5, whereby P5 binding to the BECN1 ring promotes viral replication by inducing incomplete autophagy..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.