Dogs and Wolves: What’s the Difference?

Contributed by Nadia Irfan and Joseph Birchansky

This is a graphic representation of the phylogenetic tree showing relatedness between dogs and wolves as it compares to outgroup (less related) species which branches off to form new species earlier on in history. The images show structural similarity and differences between the three species as well.

This is a graphic representation of the phylogenetic tree showing relatedness between dogs and wolves as it compares to outgroup (less related) species which branches off to form new species earlier on in history. The images show structural similarity and differences between the three species as well.

Dogs are the classic American pet, but how much do you really know about them? Dogs’ behavior is quite similar to humans’. For instance, even puppies that haven’t interacted with humans show social and cognitive skills on par with human children. This is surprising, considering their closest relative in the wild is the wolf, which is known to be more aggressive and less compatible with people. Wolves raised by humans don’t develop the same mental and social skills that domesticated dogs do. In addition, dogs are less fearful and more playful than wolves. This divergence is due to artificial selection by humans over many generations, which has resulted in dogs with improved tameness and temperament, which were reinforced by a population bottleneck – a significant reduction in population size.

Ancestors with dog-like characteristics originate in the fossil record up to 33,000 years ago. It appears dogs were first domesticated about 16,000 years ago, which actually happened before the development of agriculture. They then completely diverged from wolves 14,000 years ago, and there is evidence suggesting that dogs emerged from a single species of ancestral wolf. This divergence occurred via bottlenecks, significant reductions in population size, in both species, which were especially pronounced in dogs, from 32,000 to less than 2,000 individuals – a 16-fold reduction – and less so in wolves, which only experienced a threefold reduction. It is unclear why this reduction in wolves occurred, but it happened before humans began intentionally hunting them.

It’s interesting that, with so many behavioral and physical differences, dogs and wolves actually have very similar genomes. What’s different is which genes are being expressed, including those involved with cognition, memory, growth, and social skills. These differences in gene expression are driven in large part by artificial selection. Humans also influenced the morphology of dogs, including coat color variation, reduced cranial volume, and smaller skeletal size. These changes in morphology could potentially be deleterious because a possible effect of artificial selection may be a reduction in purifying selection, which ordinarily eliminates characteristics that are unfavorable in the wild. Research shows that humans may also have selected for behavioral traits, and these traits may have been selected for even before morphological traits. Not only did humans select for behavioral traits but food, shelter, and water availability given to them by humans are specifically responsible for differences in hypothalamic gene expression – a region associated with behavior and intelligence.

As a result of these selective pressures dogs have evolved different pack mentalities than wolves. Whereas wolves have a pair-bonded family unit that collaborates in hunting and rearing babies, dogs are less inclined to stay with one mate, are less active in raising their young, and are more dependent on human-provided resources. Overall, dogs’ and wolves’ different social, behavioral, and physical characteristics reflect speciation and domestication.

Also see: Who Helped the Dogs Evolve?

For more information, please refer to the following sources:

Albert, F.W., et al. 2012. A Comparison of Brain Gene Expression Levels in
Domesticated and Wild Animals. PLOS Genetics 8:9.

Freedman, A.H., et al. 2014. Genome Sequencing Highlights the Dynamic Early
History of Dogs. PLOS Genetics 10:1.

Li, Y., et al. 2013. Artificial Selection on Brain-Expressed Genes during the
Domestication of Dog. Molecular Biology and Evolution 30:8. 1867-1876.

Marshall-Pescini, S., Viranyi, Z, & F. Range. 2015. The Effect of Domestication on
Inhibitory Control: Wolves and Dogs Compared. PLOS ONE 10:2.

Ramirez, O., et al. 2014. Analysis of structural diversity in wolf-like canids reveals
post-domestication variants. BMC Genomics 15:.

Saetre, P., et al. 2004. From wild wolf to domestic dog: gene expression changes in
the brain. Molecular Brain Research 126:2 198-206.

Zhang, H. & Chen, L. 2011. The complete mitochondrial genome of dhole Cuon alpinus:
phylogenetic analysis and dating evolutionary divergence within canidae. Molecular
Biology Reports 38. 1656

Evolution in Influenza

Contributed by Runako Aranha-Minnis

Evolution is not only limited to the organisms we are able to see with the naked eye. Viruses like influenza are able to evolve, and this can be very dangerous to human populations. Though it is true that influenza is not the danger that it once was, it still can not be ignored. Viral resistance to treatment can lead to many deaths globally, especially during flu seasons. During these times, doctors usually see a rise in cases of viruses resistant to the treatments available at the time. One type of resistance that influenza can develop is Oseltamivir resistance. Oseltamivir is an important antiviral defense against the flu. It is found in drugs like Tamiflu, and can be rendered ineffective if resistance is developed.

Influenza and its neuraminidase

The DNA change that in the virus that occurs is related to the neuraminidase enzyme activity. The enzyme cleaves salicylic acid moieties that can be bound by the viral hemagglutinin. In essence the enzyme’s job is to help release newly formed viral particles. Imagine the enzyme as little Pac-Men just going about and eating the connections of new virus particles to let them spread. Oseltamivir works by inhibiting the activity of the neuraminidase enzyme. This limits the infectiousness of the virus.

Resistance requires changes in the DNA of the virus. Mutations, changes in the DNA, can change genes, often leading to changes in the organism. For Oseltamivir resistance, a point mutation, the change of a single base of DNA, is all that is necessary. A change in the genes leads to a change in the amino acids produced. This change in the amino acids is just one amino acid at the 274th spot in the chain leads to a change in the activity of the virus. This line of reasoning is why the mutation is called H274Y.

The H274Y mutation that gives influenza resistance usually does not spread through the population.  In early clinical tests, the mutation meant the virus was unaffected by oseltamivir, but had associated decreased viral fitness. So even though viruses with resistance would be selected for, their lower chance of survivability because of the mutation meant it did not matter. The influenza virus is able to evolve with Oseltamivir only when an associated mutation occurs. These associated mutations that allow oseltamivir resistance to keep going are permissive mutations. More recently, permissive mutations have arisen that allow influenza to be resistant to Oseltamivir without losing any fitness. Imagine a population of influenza like a game of “Where is Waldo?”:

No permissive mutations. In the absence of permissive mutations, all viruses, including Waldo, die. 

With permissive mutations. If Waldo has a permissive mutation, he survives to reproduce and the whole populations becomes Waldos because all other viruses died. 

Waldo in the first cartoon has H274Y with no permissive mutations. Without permissive mutations, there is no evolution under treatment. After treatment, the viruses are killed. There are no viruses left so the picture goes black. In the second cartoon, With permissive mutations, there is evolution for Waldo and a new viral population arises. This population only has Waldo because only Waldo has the H274Y mutation that conferred resistance.

For Further Reading:

Jesse D. Bloom, Lizhi Ian Gong, David Baltimore. 2010. Permissive Secondary Mutations Enable the Evolution of Influenza Oseltamivir Resistance Science. 328: 1272-1275

Nicholas Renzette, Daniel R. Caffrey, Konstantin B. Zeldovich, Ping Liu, Glen R. Gallagher, Daniel Aiello, Alyssa J. Porter, Evelyn A. Kurt-Jones, Daniel N. Bolon, Yu-Ping Poh, Jeffrey D. Jensen, Celia A. Schiffer, Timothy F. Kowalik, Robert W. Finberg, Jennifer P. Wang. 2013. Evolution of the Influenza A Virus Genome during Development of Oseltamivir Resistance In Vitro 88: 272-281

HIV/AIDS and the Evolution of Drug Resistance

Contributed by June Tzu-Yu Liu, Akanksha Samal and Amy Jeng

“Currently, the CDC estimates that more than 1.1 million people in the United States are living with HIV infection and around 180,900 people are unaware that they are infected. It has been observed that people diagnosed with HIV are increasing annually, around 50,000 new incidences per year.”  –

What is HIV? What is AIDS?

HIV (Human Immunodeficiency Virus) is a retrovirus that attacks the human immune system, more specifically, CD4+ T cells. These cells are essential components of the body’s defense system against infections and diseases. HIV invades T cells, uses them for replication and destroys them. The terms HIV and AIDS are often used interchangeably, however there is an important distinction. HIV is the name of the retrovirus that invades cells, while AIDS (Acquired Immunodeficiency Syndrome) is the most advanced stage of the HIV infection. People with healthy immune systems are able to fight off infections, however, people with HIV have compromised immune systems and are highly susceptible to opportunistic infections. Opportunistic infections refer to infections that do not cause serious health threats in healthy individuals, but cause life threatening illnesses in HIV positive individuals.

How does HIV replicate?

HIV mainly targets the T CD4+ cells in our bodies. When HIV enters the host, it binds to receptors on the surface of T cells. It is analogous to using a key to unlock a door. If the HIV has the right key, it can fuse with the T cell and release its genetic material into the cell. The genetic material in HIV is RNA, thus it must change its genetic material into DNA so that the host cell can replicate the genetic material. An enzyme called reverse transcriptase changes RNA into DNA. The virus’ genetic material can now integrate with the host’s. The host cell will unknowingly replicate the virus’ genetic material. Then, the virus will push itself out of the host cell, killing it in the process.

Drug Resistance?

There is high genetic diversity in HIV because of its rapid replication and high mutation rate. Currently, doctors are using a combination of different antiretroviral drugs to inhibit various steps in the HIV life cycle, leading to a synergistic effect. One major drawback to this approach, however, is drug resistance.  Scientists have found that using antiretroviral therapy (ART) increases the rate of drug resistance. According to a case study from China, prevalence of drug-resistant variants in therapy patients increased significantly to 45.4% in three months and 62.7% in six months. Alarmingly, drug resistant variants can replace the wild type variants completely within 14-28 days of treatment. Similar results were found in a case study in South Africa in which a large percentage of patients who did not respond to treatment harbor viruses with drug-resistance mutations. The effectiveness of therapeutic regimens to control the HIV pandemic are compromised due to drug resistance.

A common misconception is that evolution is a chance event. Evolution of HIV is not a chance event; it is driven by drug selective pressures. Also, organisms are commonly perceived as  getting “better” through evolution. The HIV virus isn’t getting better. It’s becoming more adapted to it’s environment. Resistant HIV is not “better” than the non-resistant strains. They have just evolved to be better suited for their environment.

For more information please see the following papers:

Hegreness, M. et al. 2008. Accelerated evolution of resistance in multidrug environments. Proceedings of the National Academy of Sciences of the United States of America 105 (37): 13977-13981.

Li, J.Y., et al. 2005. Prevalence and evolution of drug resistance HIV-1 Variants in Henan, China. Cell Research 15: 843–849.

Mammano, F., et al. 2000. Retracing the Evolutionary Pathways of Human Immunodeficiency Virus Type 1 Resistance to Protease Inhibitors: Virus Fitness in the Absence and in the Presence of Drug. Journal of Virology 74 (18): 8524-8531.

Mansky, L. M. 2002. HIV mutagenesis and the evolution of antiretroviral drug resistance. Drug Resistance Updates 5 (6), 219-223.

Marconi, V.C. et al. 2008. Prevalence of HIV-1 Drug Resistance after Failure of a First Highly Active Antiretroviral Therapy Regimen in KwaZulu Natal, South Africa. Clinical Infectious Diseases 46: 1589-1597.

Peeters, M., et al. 2002. Risk to Human Health from a Plethora of Simian Immunodeficiency Viruses in Primate Bushmeat. Emerging Infectious Disease 8: 451-457.

Sarkar, I., et al. 2007. HIV-1 Proviral DNA Excision Using an Evolved Recombinase. Science 316: 1912-1915.

Smith, R. J., et al. 2010. Evolutionary Dynamics of Complex Networks of HIV Drug-Resistant Strains: The Case of San Francisco. Science 327: 697–701.